smkoing and oral health

accomplished by
zainab noman abid
srour adel maleeh
noor mansour hasoon

supervised by
dr . zahraa al_motery
dr . rasha al_warid

introduction:
the epidemic of tobacco use is one of the greatest threats to global health today.
approximately one-third of the adult population in the world use tobacco in some
form and of who half will die prematurely. according to the most recent estimate by
the world health organization
(who), worldwide 4.9 million people died in the year 2000 as a result of thei
r addiction to nicotine.in addition to several other chronic diseases, tobacco use is a
primary cause of many oral diseases and adverse oral conditions. epidemiological
studies in india have shown that up to 80% of oral cancer patients are tobacco users.
nicotine is found in substantial amount in tobacco products that makes addicts out of
tobacco users. it is a stimulant with properties similar to those of cocaine and
amphetamines. nicotine is thousand times more potent than alcohol, 10-100 times
more potent than barbiturates and 5-10 times more potent than cocaine
or morphine in its addictive potential. the addictive effect of nicotine is linked to its
capacity to trigger the release of dopamine- a chemical in the brain that is associated
with feelings of pleasure. however, recent research has suggested that in the long
term, it depresses the ability of the brain to experience pleasure. so, smokers and
chewers need greater amounts of the drug to achieve the same levels of satisfaction.
tobacco use is therefore a form of self medication further use relieves the withdrawal
symptoms, which set in soon after the effects of nicotine wear off (1).
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 (4, 5),and with oral
malignancies (6, 7). several recent documents have reviewed the scientific evidence
relating to the oral disease burden attributable to tobacco use (8) and have highlighted
the role and the need for the dental profession to get involved with
tobacco intervention (9).smoking cause’s discoloration of teeth and some argue that
tobacco in fact might increase dental decayes it lowers salivary ph and the
buffering power.smoking is likely to cause halitosis and may affectsmell and taste.
smokers may present with generalized melanosis of the oral mucosa that
often necessitateinvestigations 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 (10-11). 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 (5). 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
does smoking cause other changes in the mouth?
• smoking causes staining of the teeth and bad breath. quitting will help to
prevent further staining and can improve the smell of the breath.(3)
one of the effects of smoking is staining of your teeth. this is caused by the tar and
nicotine in the cigarettes. smoking can make your teeth yellow in a short period of
time and people who have smoked for many years often complain that their teeth are
brown in colour and this is due to the staining from tobacco.(3)
• smoking can dull taste buds and make food taste bland by changing the blood supply
your taste buds are getting.(3). quitting allow taste food again.
• smokers have reduced blood flow to their gums. if the person smoke it takes longer
to heal after an injury or surgery to his\her mouth. gum disease is a bacterial infection
of the gum tissue. it s caused by the buildup of plaque and tartar on the teeth, but
smoking also plays a major role. smokers have twice the risk of developing gum
disease. this is because nicotine constricts your blood vessels, and reduced blood flow
impairs your gum tissue s ability to fight infections. plus, this reduced blood flow
makes it harder for your gums to heal from damage, so treatments for gum disease
may not work as well. quitting means a better recovery and a shorter healing time.(11)
• smokers can also get ‘smoker’s palate’ or nicotine stomatitis . smokers develop a
pale or white roof of the mouth, often with red dots. nicotine stomatitis is usually seen
in pipe smokers and reverse cigarette smokers (when the lit end of the cigarette is
placed in the mouth). it is probably due to the concentrated heat stream hitting the roof
of the mouth. less commonly it develops with cigarette or cigar smoking and rarely
with drinking extremely hot liquids. the combination of hot drinks and smoking may
increase the risk.
men and women develop nicotine stomatitis, but as pipe smoking is more common
with men, so nicotine stomatitis shows a male predominance.(13)
smoker’s palate can disappear when you quit smoking.
• smoking inhibits the ability of saliva to break down bacteria and food products in the
mouth. when harmful effect of cigarettes impacts the salivary glands, the first to be
affected is parotid gland whose role is secretion of watery saliva. the loss of its
function is compensated by submandibular and sublingual glands which secrete
mucous saliva. this explains thicker saliva in smokers. recent research confirms that
smoking negatively affects the quality of saliva. substances from cigarette smoke
destroy protective macromolecules of saliva, enzymes and proteins, and thus saliva
loses its protective role and becomes an agent in carcinogenesis and development of
oral and oropharyngeal cancer . |(15) quitting allows saliva to recover and continue
protecting the mouth.
smoking and dental caries
smoking and its relation to dental caries is a subject of many opinions. from early
reports in literature and a common belief was that smoking actually helps to reduce
dental caries (9, 10, 11). schmidt, in 1951, supported this belief when he reported that
increase in tobacco smoking was followed by a decrease in caries rate (12). the
concentration of thiocyanate, a constituent of tobacco smoke and normal saliva with
possible caries-inhibiting effect, was found to be higher in smoker’s saliva (13). so,
one might predict less dental caries in smokers. on the other hand, the decreased
buffering effect and possible lower ph of smoker’s saliva and the higher number of
lactobacilli and streptococcus mutans may indicate an increased susceptibility to
caries (13, 14). in addition, results also showed no significant differences in salivary
flow rates between smokers and non-smokers (8). to date, quite a few investigators
have discovered a correlation between elevated smoking level and dental caries (16,
17, 18). for example, in 1952, ludwick and massler reported that those who smoked
more than 15 cigarettes a day had significantly higher number of decayed, missing,
and filled teeth (19). in 1971, ainamo found that increased smoking resulted in
significantly higher number of decayed surfaces per dentition and also noted a
trend toward more missing surfaces and fewer restored surfaces in subjects with a high
consumption of cigarettes (20). in 1990, zitter bart confirmed association between
smoking and the prevalence of dental caries in adult males. smokers had significantly
higher dmft (decayed, missing, and filled teeth) score, untreated decayed surfaces,
and missing surfaces. he further correlated that more cigarettes consumed per day
resulted in more missing tooth surfaces in a smoker’s mouth (11). a swedish study
carried out in 1991 shows that smoking, as a habit and an increased number
of cigarettes smoked per day, are positively correlated with increased in number of
decayed, missing and filled teeth (21).
even though a recent study done on american female population in 2006 did not
establish a causative relationship, cigarette smoking was shown to be associated with
the prevalence of caries (22). studies in this regard have considered multiple variable
factors which can contribute directly or indirectly to the increase in the incidence of
dental caries in smokers such as age, tobacco habits other than smoking, oral hygiene
habits, eating habits, drinking habits, preventive visits to dentist (dental recalls) and
overall health standards. due to these factors, it is difficult to conclude the association
between a single positive factor which can cause increase in caries incidence in
smokers, therefore, it is not easy to establish the strength of relationship between
smoking and dental caries.association between smoking and dental caries is well
documented in older age groups (23, 24). among middle-age (15) or young adults (25)
results are inconsistent. non-smokers reported more frequent healthy oral health
behavior than did daily smokers(26). studies indicate that smokers not only had bad
oral hygiene and less primitive outlook on health, but also had different eating habits,
presumably consuming high amount of sugar containing products like soft drinks and
snacks (15, 21). daily smoking was associated with increased use of sugar in tea or
coffee, and with more frequent alcohol consumption (26). it is also seen that smokers
have ineffective brushing habits than non-smokers (20, 27, 28). the distribution of
brushing strokes around the mouth was more uniform in the non-smokers than in the
smokers, which may indicate a tendency towards less favorable tooth brushing
performance in smokers (29).
and current smokers were less likely to report regular preventive visits to dentists and
were reluctant to use accessory dental aids such as dental floss. current smokers also
had higher scores on the dental attitudes scale, indicating that a lower value is placed
on retaining natural teeth (23). in natural tobacco, sugar can be present in a level up to
20%wt. in addition, various sugars and sweeteners are added intentionally during
tobacco manufacturing process up to 4%wt or can be up to 13%wt of sugars. sugars
used as cigarette additive include glucose, fructose, invert sugar (glucose/fructose
mixture) and sucrose. in addition, many tobacco additives contain high amount of
sugars.for example, fruit juices, honey, molasses extracts, cones and maple syrup and
caramel. the added sugars are usually reported to serve as flavor /casing and
humectants. however, sugars also promote tobacco smoking, because they generate
acids that neutralize the harsh taste and throat impact of tobacco smoke.moreover, the
sweet taste and the pleasant smell of caramelized sugar flavors are appreciated in
particular by starting adolescent smokers (30). all the above findings can contribute to
an increased prevalence of dental caries among smokers. however, a direct etiological
relation between smoking and dental caries is still missing. the above-mentioned
studies and findings point to the assumption that smoking has some influence on high
caries incidence. further studies, clinical trials and experiments are therefore needed
to elucidate the independent effect of smoking as one of the causes of dental caries.
numerous epidemiological studies around the world have reported a close relationship
between smoking and the occurrence of dental caries. in italy, smoking military
personnel (including 94.6% men and 5.4% women) have a higher decayed, missing,
filled teeth (dmft) score than non-smoking personnel1. in finland, daily smoking
has been found to increase 4-year caries experience in adults (31). a study in scotland
has shown that if a pregnant woman smokes it might result in her child having a
higher prevalence of caries than a child born to a non-smoking mother (32).
in portugal, smoking has been confirmed as a risk factor for dental caries, and
avoiding exposure to smoking leads to a 7% decrease in caries incidence(33). a
systematic review by benedetti et al.5 also verified that tobacco smoking had a close
association with an increased risk of caries. however, there were differences between
smokers and non-smokers in regard to personal education and economic situation(34).
investigation showed that smokers tended to have bad eating habits, payed less
attention to oral self-care, rarely seeking professional medical treatment and had poor
compliance after treatment7-9. all these behaviors 6-9 mentioned above could
increase the incidence of caries. further evidence to verify the cariogenic mechanisms
of smoking needs to be researched. nowadays, researchers have found that smoking
has an effect on caries-related bacteria (34).
the influence of cigarette products on the growth of oral bacteria
it is well known that bacteria create the preconditions for caries. bacteria in the oral
cavity produce acid by degrading the fermentable carbohydrates through the secretion
of enzymes or metabolism, so as to induce further demineralization of dental hard
tissues(35). an early study11 in 1991 claimed that smoking inhibited the growth of
gram-positive cocci including neisseria, one of the early colonizers in dental plaque.
smokers were considered to be inclined to form gram-negative bacterial colonization
in their oral cavity, which was contradicted by later research. baboni et al.(36) found
that cigarette smoke condensate promoted the adhesion of streptococcus mutans and
candida albicans to the acquired pellicle on orthodontic materials. zonuz etal.(37)
incubated s. mutans and streptococcus sanguis (now known as
streptococcus sanguinis) in atmospheric air, carbon dioxide and cigarette smoke. they
found that cigarette smoke enhanced the growth of both bacteria strains, but
s. mutans was affected more. one possible reason was that the former study did not
examine the main cariogenic bacteria such as s. mutans. another reason might be that
there were differences in the experimental conditions, for example, different bacteria
strains, cigarette varieties, different exposure time and so on. in addition, in vitro
culture could not completely mimic the growth of bacteria in vivo .
there are about 7000 different kinds of molecules inhaled from smoking cigarettes14,
making it difficult to ascertain the component that has the greatest effect on cariesrelated bacteria. more than 30 years ago, researchers believed it was the sugar content
in tobacco that supported and influenced the growth of s. mutansand s. sanguinis,
while chemical components including nicotine in tobacco did not affect oral
microflora(38). nowadays, more and more evidence indicates that nicotine, the main
bioactive and addictive substance in cigarette products, has a major impact on cariesrelated bacteria.
smoking and its effect on the periodontium and periodontal therapy
periodontal disease is defined as inflammatory destruction of periodontal tissue and
alveolar bone supporting the teeth. progression and severity of the disease depends on
complex interactions between several risk factors such as microbial, immunological,
environmental and genetic factors, as well as age, sex, and race. .(39)
pindborg (1947) was one of the first investigators to study the relationship between
smoking and periodontal disease. (40) increased prevalence and severity of
periodontal destruction. – on average, smokers are 4 times likely to have periodontal
disease as compared to person who had never smoked. (41)– former smoker were 1.7
times more likely to have periodontitis than person who had never smoked – older
adults are approximatelty 3 times more likely to have severe periodontal disease and
number of pack years of tobacco use is significant factor in tooth loss, coronal root
caries and periodontal disease. – cigarette smoking is associated with increased
severity of generalized aggressive periodontitis i young adults. – smokers between the
age of 19-30 years are 3.8 times more likely to have periodontitis than non smoker.
(42)
women from ages 20 to 39 and men from ages 30 to 59 who smoke cigarettes have
twice the chance of having periodontal disease or becoming edentulous as do nonsmokers the effects of smoking on periodontal status to be more pronounced in
younger women. (43)
prevalence of moderate and severe periodontitis
• current smokers – 25.7% • former heavy smokers – 20.2% • cigar/pipe smokers –
17.6% • non-smokers – 13.1%
•deeper probing depths and a larger number of deep pockets (44)
figure 45
• more attachment loss including more gingival recession .
smokers are more than 6 times as likely as non smokers to demonstrate continued
attachment loss .
the prevalence of moderate and severe periodontitis and percentage is more severe in
current cigarette smoker .
cigar and pipe smoker showed a severity of disease.
_more alveolar bone loss _
over a 10 year period bone loss has been reported to be twice as rapid in smokers as
in non smokers. – proceeds more rapidly even in presence of excellent plaque control
(46)

figure 47
more tooth loss
– young individuals smoking more than 155 cigarettes/day shows highest rate of tooth
loss ) – tooth loss is increase in cigar and pipe smoker as compared to non
smoker (48)
increased prevalence of periodontal disease with increased number of cigarettes
smoked/day. • decreased prevelance and severity with smoking cesation – risk of
periodontitis decreases with the increasing number of years since quitting smoking –
negative effects of smoking on host are reversible with smoking cesation and
therefore, smoking ceastion should be integral part of periodontal education and
therapy (49)
effects of smoking on etiology and pathogenesis of periodontal
disease:-
* • the increased prevalence and severity of periodontal destruction associated with
smoking suggests that the host- bacterial interactions normally seen in chronic
periodontitis are altered, resulting in more aggressive periodontal breakdown. (50)
• this imbalance between bacterial challenge and host response may be caused by –
changes in the composition of the subgingival plaque, – with increases in the numbers
and virulence of pathogenic organisms, – changes in the host response to the bacterial
challenge, – or a combination of both. (51)
*microbiology •
smokers may have higher levels of plaque than nonsmokers, which may be accounted
for by poorer levels of oral hygiene rather than higher rates of supragingival plaque
growth
). • several studies have shown that smokers harbor more microbial species which are
associated with periodontitis than non-smokers, including – p. gingivalis, –
a. actinomycetemcomitans, – tanerella forsythia (bacteroides forsythus) (zambonet
al. 1996), • smokers are 2.3 times more likely to harbour t. forsythia than non
smokers and former smokers – p. intermedia, – peptostreptococcusmicros, –
fusobacterium nucleatum, campylobacter rectus), – staphylococcus aureus, –
eschericia coli, and – candida albicans .
increased colonization of shallow periodontal pockets by periodontal pathogens. •
smokers may have a higher proportion of sites harboring these putative periodontal
pathogens, in particular the palatal aspects of the maxillary teeth and the upper and
lower incisor regions (haffajee & socransky2001a,b). • in contrast several studies
have failed to show differences in the bacterial species between smokers and nonsmokers (52)
schematic summary of clinical findings of subgingival
microflora in smokers.53
immune-inflammatory response effects on pmn function •
smokers have an increased number of leukocytes in the systemic circulation ), but
fewer cells may migrate into the gingival crevice/pocket . • studies in vitro have
shown a direct inhibition of neutrophil and monocyte–macrophage defensive functions
by high concentrations of nicotine that may be achieved in patients using smokeless
tobacco . 1995). • macfarlane and co-workers (1992) demonstrated abnormal pmn
phagocytosis associated with a high level of cigarette smoking.
neutrophil defects have been associated with an increased susceptibility to
periodontitis, including cyclic neutropenia where there is a reduction in the number of
neutrophils, and conditions such as leukocyte adhesion deficiency (lad 1 and lad
2), which may be responsible for cases of generalized prepubertal periodontitis as
described by page et al. (1983). • neutrophils obtained from the peripheral blood, oral
cavity, or saliva of smokers or exposed in vitro to whole tobacco smoke or nicotine
have been shown to demonstrate functional alterations in – chemotaxis, –
phagocytosis, and – the oxidative burst (54)
proposed mechanisms for negative periodontal effects of smoking
vascular alteration
altered neutrophils function
decreased lgg production
decreased lymphocytes proliferation
increased prevalence of periopathogens
altered fibroblsat attachment and function
difficulty in eliminating pathogens by mechanical therapy
negative local effects on cytokine and growth factor production (55)
smoking and periodontitis in young adults (?35 years)
* several studies have shown young adult smokers aged 19-30 years had a higher
prevalence and severity of periodontitis compared to non-smokers despite similar or
lower plaque levels. the prevalence of periodontitis, defined as having a site with
attachment loss of ?2 mm and probing depths of ?4 mm, was three to four times
higher in young smokers compared to non-smokers (56)
smoking and periodontitis in adult
current smokers have deeper probing depths, greater attachment loss, more bone loss,
and fewer teeth.
smokers also exhibit more supragingival calculus deposits.
.smokers were four times more likely to have periodontitis as compared to nonsmokers.
*among 20-49 year-olds, the adjusted odds ratio for a mean attachment loss of 1 to
1.99 mm among current smokers was 2.29, whereas the odds ratio for attachment loss
?3 mm was over 18.(57).
figure 58
this suggests smoking is particularly important in etiology of sever periodontal
attachment loss.
there is a strong dose-response relationship between the amount smoked and the
severity of periodontal destruction which further supports the role of smoking as a risk
factor for periodontitis. the most marked difference between smokers and nonsmokers in probing depths or attachment loss occurs in the maxillary lingual area and
mandibular anterior area, suggesting a local effect of smoking. (59)
the effect of smoking on periodontal therapy:-
non-surgical and surgical therapy :-
numerous studies have shown smoking compromises probing depth and/or attachment
gain outcomes following non-surgical or surgical therapy. the numerical differences
between smokers and non-smokers become more pronounced in probing depths ?5
mm, where smokers demonstrated 0.4 mm to 0.6 mm less improvement in clinical
attachment levels following scaling and root planning. following flap debridement
surgery, smokers experienced upto 1 mm less improvement in clinical attachment
levels in probing depths that were initially ?7mm.(60)
figure 61
mechanism of action of smoking on periodontal tissues :-

a study by hanioka et al.26 showed that smoke contains carbon monoxide
which will lower the oxygen saturation of haemoglobin in healthy gingiva. the same
study also showed that oxygen tension within the pockets was significantly reduced in
smokers. this may favour the growth of anaerobic bacteria, even in the shallower
pockets. smoking extends a favourable habitat for periodontal pathogens such as
formerly porphyromonas gingivalis, aggregatobacter actinomycetemcomitans
actinobacillus actinomycetemcomitans) and prevotella intermedia in shallow pockets
of less than 5 mm.62. it was also found that those pathogens were more prevalent in
maxillary teeth and upper and lower incisors.63however, in a study using oral
mucosal and saliva bacterial samples taken from smokers and non-smokers diagnosed
with chronic periodontitis, it was reported that there was only a small but not
statistically significant difference in the proportions of bacterial species between
smokers and non-smokers. (64)
smoking and oral cancer
oral cancer
the risk of oral cancer is about 5 to 10 times greater among smokers compared to
people who never smoked(65). this risk is further multiplied among smokers who also
drink alcohol(66).
smokers are at higher risk of dying from oral cancer than those who have never
smoked. the risk of dying from oral cancer increases with the amount smoked per
day(67) .thirty-seven percent (37%) of people diagnosed with oral cancer are
expected to die within 5 years after diagnosis(68). there were 1,108 deaths from oral
cancer in canada in 2007(69).
research has shown that in 2002, about half of oral cancer deaths were due to
)70 (smoking .
oral cancer is uncontrolled growth of abnormal cells starting in the mouth cavity
leading to the formation of a tumor. development of oral cancer occurs predominantly
on the tongue, lower lip and floor of the mouth.
squamous cell carcinoma is the most common cancer of the oral cavity. in men, most
oral cancers are found on the floor of the mouth and tongue in women, the most
common sites are the tongue and gums(71).
mechamism of action of smoking on oral cancer :
although several tobacco agents play a role in the development of tumors, the potent
effects of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (nnk) and n -
nitrosonornicotine (nnn) are unique. metabolically activated nnk and nnn induce
deletingrious mutations in oncogenes and tumor suppression genes by forming dna
adducts, which could be considered as tumor initiation(72). meanwhile, the binding of
nnk and nnn to the nicotinic acetylcholine receptor promotes tumor growth by
enhancing and deregulating cell proliferation, survival, migration, and invasion,
thereby creating a microenvironment for tumor growth. these two unique aspects of
nnk and nnn synergistically induce cancers in tobacco-exposed individuals. this
review will discuss various types of tobacco products and tobacco-related cancers, as
well as the molecular mechanisms by which nitrosamines, such as nnk and nnn,
induce cancer(73)
chemical carcinogenesis: chemical agents, e.g.: tobacco, tannins, asbestos, heavy
metals, alcohol abuse. (alcohol by itself is not a carcinogen but it promotes the effect
of tobacco and may affect the immune response sec?ndary to liver damage. the risk
for tobacco-induced cancer is increased by 100- fold with the abuse of both tobacco
and alcobol.) carcinogenesis caused due to chemicals occurs in stepwise manner.
it goes through the following stages
initiation: this is the induction of certain irreversible changes within the dna of the
cells. initiated cells do not become different from their parent cells structurally or
functionally. these cells however have the ability to give rise to tumors if stimulated
by promoting agents. the damage caused to the dna is critical when protooncogenes
or recessive cancer genes are altered.(74)
promotion: chemicals which promote tumor formation in cells that have previously
been initiated are referred to as promoting agents. promoting agents by themselves are
not capable of causing tumors in uninitiated cells. their effect on cells short-lived and
reversible. these promoting agents bring about differentiation of initiatod cells.(75)
figure (1): mechanism of action of smoking and oral cancer (76)
oral squamous cell carcinoma (oscc) is commonly preceded by oral potentially
malignant disorders. glucose transporter-1 (glut-1) protein expression is up
regulated in malignant cells that show increased glucose uptake. alterations in glut1 expression have been reported in several potentially malignant and malignant
lesions(77)
oral carcinogenesis is a complex process that causes alterations in various genes
these genetic alterations produce altered proteins. in recent years, there is
overexpression of altered proteins related to cell metabolism that has a role in the
development of oscc and also in the progression of oed to oscc(55). glucose
homeostasis within the body is predominantly maintained by the glucose transporter
(glut) protein family comprising 14 isoforms. increased expression of certain
members of glut protein family has been reported in various cancers such as lung,
pancreas, prostate and esophagus, suggesting that the tumor cells use glycolytic
pathway for their long-term maintenance and can proliferate very rapidly even in low
oxygen tension environment for their survival. glut-1 glucose transporter is a trans
membrane glycoprotein that is involved in na+-independent transport of glucose into
cells. studies revealed alterations in glut-1 expression in several potentially
malignant and malignant lesions (78)
symptoms of oral cancer include red or white spots in the mouth, which may become
open sores, facial asymmetry swelling/ulceration, lymph nodes enlarged, induration-
usually present in a malignant ulcer or swelling and loss of sensation over the
distribution of the inferior alveolar nerve or infraorbital nerve (79)
clinical representation of oral squamous carcinoma
1- exophytic (mass forming fungating, papillary, verruciform)
2- endophytic (invasive, ulcerated
3- leukoplakic (white patch)
4- erythroplakic (red patch)
5- erythroleukoplakic (combined)
oral squamous cell carcinomas (oscc) account for >90% of all oral cancers. it can
arise either de novo or from oral potentially malignant disorders that include oral
leukoplakia, erythroplakia , oral lichen planus and oral sub mucous fibrosis that
histologically represent the oral epithelial dysplasia (oed)(80).
oral leukoplakia and erthroplakia
(ol) is a disorder of the white lesion group, which is diagnosed by the exclusion
method. additionally, ol is a clinical term used to describe white plaques of
questionable risk, which does not fall under any other classification of this group(81)
.the prevalence of ol is of 1 to 4% in the world population, being the opmds are
more common, representing 85% of these lesions .this disorder’s clinical aspect
represents two types, classified as homogeneous or non-homogeneous ol
microscopically, it may present different histological degrees in its tissue architecture,
ranging from simple hyperkeratosis to grades of oral epithelial dysplasia (oed), or to
carcinoma itself. the oed is an alteration whose severity is an indicator of
malignancy thus, progressing of a standard epithelium to opmds(82). the diagnostic
criteria are essential since it decreases the risk of malignant transformation of the
lesion. examination of the oral cavity is the primary method of detection. however,
the degree of dysplasia is determined not only by visual examination, and biopsy is
mandatory in cases of oed in leukoplakia, treatment with the elimination of risk
factors and longitudinal follow-up are essential to prevent the disorder’s progress,
favoring a good prognosis for patients. in addition to dysplasia, other clinical
predictors should be taken into account to assess the lesion’s potential to malignant
transformation(83).
erythroplakia and erythroleukoplakia are less common, but are usually more serious.
more of these red lesions (compared to white lesions or leukoplakia) turn out to be
cancer when they are biopsied or will develop into cancer later. dysplasia is a term
that might be used to describe leukoplakia or erythroplakia .it s flat or slightly raised,
red area that often bleeds easily if it s scraped..
figure (2) : oral potentially malignant cancers ,on the left we see erythroplakia on lateral border
of tongue ,
the picture on the right represent white patch that called leukoplakia (84)
figure (3) :lichen planus and submucous fibrosis in lower lip (85)
most of the oscc cases are diagnosed in advanced stages. this can be due to lack of
awareness among patients as most of the cases are painless in initial stages(86)
figure (4): on the left we see exophytic cancer tumor on lateral border of tongue, the right one
represent an endogeneous cancer tumor in retromolar pad area (87)
the link between tobacco and oral cancer :
tobacco use is known as a major risk factor for oral and many other cancers. all
tobacco products, including cigarettes, cigars, pipe tobacco, chewing tobacco, and
snuff, contain the following :
poisonous substances (toxins)
cancer-causing agents (carcinogens)
nicotine, an addictive substance
most of the agents associated with oral cancer development are also involved in the
etiology of opmds, such as chronic exposure to ultraviolet radiation, alcohol
consumption, tobacco use (smoking), nutritional deficiency, and genetic
inheritance(88)
treatment for oral cancer often involves surgery and radiation therapy. surgery
involves removal of the affected tissue and if the cancer has spread to the jaw, part of
the jawbone may also be removed. this may change how the face looks and the ability
to chew, swallow, or talk(89) .
the benefits of quitting
when people quit smoking, the risk of oral cancer starts to decrease rapidly. after 10
to 20 years of quitting, the risk decreases to almost the same level as that of someone
who has never smoked(90). quitting can also decrease the risk of developing a new,
second oral cancer in smokers with a previously treated oral cancer(91)
quitting is more effective than other measures to avoid the development of oral cancer
and other smoking-related diseases.
smoking and tooth staining
teeth stain for many reasons, including your food and drink choices, oral hygiene, and
medication use. teeth stains occur on the surface of the tooth or below the tooth
enamel and some people develop both types of teeth stains. types of tooth
discoloration (stains)tooth discoloration can occur as a result of surface stains, due to
actual changes in your tooth material, or because of a combination of both factors(92).
dental professionals have identified three main categories of tooth discoloration :
extrinsic teeth stains: an extrinsic tooth stain is staining on the surface of the tooth.
it occurs when stain particles, such as pigmented residue from food or drink, build-up
in the film of protein that covers the tooth enamel. extrinsic tooth stains are typically
caused by tobacco use or by regularly drinking coffee and tea, wine or cola drinks.
this type of tooth stain responds well to regular dental cleaning and brushing the teeth
with whitening toothpaste .
intrinsic teeth stains: an intrinsic tooth stain is staining below the surface of the
tooth. it occurs when stain-causing particles work through the exterior of the tooth and
accumulate within the tooth enamel. excessive fluoride use and also have been
associated with intrinsic, especially in children. an intrinsic tooth stain is trickier to
remove, but it can be done. an intrinsic tooth stain may require bleaching using
professional or at-home chemical teeth-whitening products, such as white strips .
age-related teeth stains: age-related teeth stains combine the results of both
intrinsic and extrinsic tooth discoloration. because the core tissue of your teeth, the
dentin, naturally yellows over time, teeth discolor with age. as we age, the enamel
that covers the tooth becomes thinner, allowing the dentin to show through. these
intrinsic causes of discoloration combined with extrinsic causes such as the effects of
certain foods, beverages, and tobacco, will cause most adults teeth to discolor with
age(93).
figure (5): difference between food stain,wine , age staining and smoking staining (94)
stained teeth causes teeth stains have many causes. certain foods and drinks can
cause teeth stains, and as we’ve talked about, tooth discoloration is also a product of
several biological factors, including the transparency of your tooth enamel.
food & drink: coffee, tea, dark sodas, red wine, and even a few fruits and vegetables
are proven causes of discolored teeth .
tobacco: both cigarettes and chewing tobacco can contribute to discolored teeth .
oral care: poor dental hygiene, such as inadequate brushing or flossing, can lead to
tooth discoloration .
trauma or disease: any trauma, illness, or disease that affects enamel development in
children—either in the womb or while teeth are developing (under the age of 8)—can
cause discolored teeth. trauma to adult teeth can also cause discolored teeth. in
addition, there are a few diseases and disease treatments that can cause discolored
teeth. chemotherapy and radiation, for example, discolor teeth(95).
mechanism of action of smoking on tooth staining
normally, the surface of the tooth enamel is covered by a thin salivary membrane
called pellicle. when tannin in black tea, green tea or coffee or cigarette tar and
nicotine bonds with calcium or metallic ions in saliva, stains are formed.
figure(6): mechanism of staining due to smoking for many years (96)
to know how to remove a tooth stain, it helps to know what type of stain you are
dealing with. paul a. sagel, a procter & gamble research fellow, has conducted
extensive research into the science of tooth stains. research by sagel and others have
shown that some stain particles remain on the tooth enamel, while others work through
the tooth enamel over time and set beneath the tooth surface, which creates dullness
.)and tooth stain(97
tobacco stains on teeth are often difficult to remove because they have occurred over
years of smoking. the stains have settled deep into the enamel and often will penetrate
.to the outer layer of the dentin
fortunately, these stains are not permanent and can be removed with professional teeth
whitening(98).
darker stains around edges of teeth :
there are 2 reasons why smokers may see darker staining around the edges of their
teeth or near the gum line :
1- tobacco stains on tooth edges
the edges of the teeth (where two teeth meet) are the primary areas where tartar builds
up. tartar is far more porous than enamel and thus will absorb the stains of nicotine
and tar much faster. people who see staining on the edges of their teeth generally do
not floss or do not get regular dental cleanings .
2- tobacco stains near gum line
another negative effect of smoking is receding gum lines. this means that the gums
begin to shrink and pull away from the teeth (thus exposing more of the root of the
tooth). roots of your teeth are not covered with same thickness of enamel and are
made up of softer, more porous dentin material. dentin will stain much quicker.
fortunately, dentin can also be whitened much faster(64).
figure (7) : tooth staining on the left show gum line staining , the right one represent tooth staining
near tooth edges (99).
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