1. The document discusses cancers of the oral cavity, including risk factors, etiology, pathogenesis, clinical presentation, diagnosis, treatment and prevention. It notes that over 90% of oral cancers are squamous cell carcinoma, which commonly present as lumps or ulcers in the lip or tongue. 2. Tobacco use, alcohol consumption, and chewing betel nut are among the strongest risk factors. HPV infection is also linked to some oropharyngeal cancers. Other risk factors include age, gender, diet, sunlight exposure, and certain medical conditions or genetic syndromes. 3. The etiology of oral squamous cell carcinoma is multifactorial but strongly related to lifestyle habits like smoking, alcohol use, and

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Ministry of Education Republic of Belarus
Vitebsk Order of Peoples’ Friendship State Medical University
Department of Stomatology
Head of the Department: O.A. Zharkov
Teacher:
Referath
Topic: Cancers of Oral Cavity. Etiology. Pathogenesis.
Clinic. Diagnosis. Treatment. Prevention of
complications. Prevention.
DinooshDe Livera
Student5th Course
Group No: 49
InternationalStudents’ TrainingFaculty
VSMU
2017’

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Background
Oral cancer is a major neoplasm worldwide and accounts for most head and neck cancers.
It theoretically should be largely preventable or detectable at an early stage. Approximately
90% of oral cancers are squamous cell carcinoma (SCC), which is seen typically on the lip
or lateral part of the tongue usually as a lump or ulcer that is white, red, or mixed white and
red. Note the image below. Any single lesion persisting for more than 3 weeks should be
regarded with suspicion. The mnemonic RULE (Red, Ulcerated, Lump, Extending for 3 or
more weeks) is an aid to diagnosis. Lip cancer maybe SCC or Melanoma.
The Oral cavity extends from the Vermillion border of the Lips to the Junction between the
Hard & Soft Palate. Oral cancer may affect the oral cavity, buccal mucosa, tongue, gingiva,
floor of mouth and hard palate.
Oral SCC (OSCC) is particularly common in the developing world, mostly in older males.
There is concern about an ongoing increase in younger patients and in women, as well as in
the oropharynx. The etiology of SCC appears to be multifactorial and strongly related to
lifestyle, mostly habits and diet (particularly tobacco alone or in betel, and alcohol
use).Other factors such as infective agents may also be implicated, particularly in
oropharyngeal cancer. Immune defects or immunosuppression, defects of carcinogen
metabolism, or defects in DNA-repair enzymes underlie some cases of SCC. Sunlight
exposure predisposes to lip cancer.
Findings from the history and clinical examination by a trained diagnostician are the
primary indicators of OSCC, but the diagnosis must always be confirmed histologically with
repeated biopsies if the clinical picture is consistent with SCC.
Oral squamous cell carcinoma in the most common intraoral site manifesting as a chronic, indurated ulcer.
Premalignant conditions include: leukoplakia, erythroplakia and submucous fibrosis.

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Risk Factors:
1. Tobacco
2. Alcohol
3. Betel quid / Gutka
4. Viruses (HPV, HSV, EBV. CMV)
5. Gender ( Males > Female )
6. Age > 55
7. UV exposure (Outdoor jobs)
8. Poor nutrition (Plummer Vinson syndrome, low intake of fruits and vegetables)
9. Weakened Immune System ( AIDS, Organ transplantation, Congenital ID)
10. Race: African-American
11. Genetic Syndromes: Fanconi’s Anemia, Dyskeratosis Congenita, Lichen planus
12. Chronic friction: Broken teeth, loose-fitting dentures
13. Candidiasis (Nitrosamines)
A risk factor is anything that changes a person’s chance of getting a disease such as cancer.
Different cancers have different risk factors. For example, exposing skin to strong sunlight
is a risk factor for skin cancer. Smoking is a risk factor for many cancers.
There are different kinds of risk factors. Some, such as your age or race, can’t be changed.
Others may be related to personal choices such as smoking, drinking, or diet. Some factors
influence risk more than others. But risk factors don't tell us everything. Having a risk
factor, or even several, does not mean that a person will get the disease. Also, not having
any risk factors doesn't mean that you won't get it, either.
Some people who have oral cavity or oropharyngeal cancer have few or no known risk
factors, and others who have several risk factors never develop the disease. Even if
someone does have risk factors, it is impossible to know for sure how much they
contributed to causing the cancer.

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Tobacco and alcohol
Tobacco and alcohol use are among the strongest risk factors for oral cavity and
oropharyngeal cancers.
Tobacco use
Most people with oral cavity and oropharyngeal cancers use tobacco, and the risk of
developing these cancers is related to how much and how long they smoked or chewed.
Smokers are many times more likely than non-smokers to develop these cancers. Tobacco
smoke from cigarettes, cigars, or pipes can cause cancers anywhere in the mouth or throat,
as well as causing cancers of the larynx (voice box), lungs, esophagus, kidneys, bladder, and
several other organs.
Pipe smoking is a particularly significant risk for cancers in the area of the lips that touch
the pipe stem.
It is important for smokers who have been treated for oral cavity or oropharyngeal cancer
to quit smoking, even if their cancer seems to be cured. Continuing to smoke greatly
increases their risk of developing a second cancer of the mouth, throat, larynx (voice box),
or lung.
Oral tobacco products (snuff or chewing tobacco) are linked with cancers of the cheek,
gums, and inner surface of the lips. Using oral tobacco products for a long time poses an
especially high risk. These products also cause gum disease, destruction of the bone sockets
around teeth, and tooth loss. It is also important for people who have been treated for oral
cavity or oropharyngeal cancer to give up any oral tobacco products.
Drinking alcohol
Drinking alcohol increases the risk of developing oral cavity and oropharyngeal cancers.
About 7 out of 10 patients with oral cancer are heavy drinkers.

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Drinking and smoking together
The risk of these cancers is even higher in people who both smoke and drink alcohol, with
the highest risk in heavy smokers and drinkers. According to some studies, the risk of these
cancers in heavy drinkers and smokers may be as much as 100 times more than the risk of
these cancers in people who don’t smoke or drink.
Betel quid and gutka
In Southeast Asia, South Asia, and certain other areas of the world, many people chew betel
quid, which is made up of areca nut and lime wrapped in a betel leaf. Many people in these
areas also chew gutka, a mixture of betel quid and tobacco. People who chew betel quid or
gutka have an increased risk of cancer of the mouth.
Human papilloma virus (HPV) infection
Human papilloma virus (HPV) is a group of more than 150 types of viruses. They are
called papilloma viruses because some of them cause a type of growth called a papilloma.
Papillomas are not cancers, and are more commonly called warts.
Infection with certain types of HPV can also cause some forms of cancer, including cancers
of the penis, cervix, vulva, vagina, anus, and throat. Other types of HPV cause warts in
different parts of the body.
HPV can be passed from one person to another during skin-to-skin contact. One way HPV is
spread is through sex, including vaginal and anal intercourse and even oral sex.
HPV types are given numbers. The type linked to throat cancer (including cancer of the
oropharynx) is HPV16.
Most people with HPV infections of the mouth and throat have no symptoms, and only a
very small percentage develop oropharyngeal cancer. Oral HPV infection is more common
in men than in women. In some studies, the risk of oral HPV infection was linked to certain

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sexual behaviors, such as open mouth kissing and oral-genital contact (oral sex). The risk
also increases with the number of sexual partners a person has. Smoking also increases the
risk of oral HPV infection. At this time the US Food and Drug Administration has not
approved a test for HPV infection of the mouth and throat.
The number of oropharyngeal cancers linked to HPV has risen dramatically over the past
few decades. HPV DNA (a sign of HPV infection) is now found in about 2 out of 3
oropharyngeal cancers and in a much smaller fraction of oral cavity cancers. The reason for
the rising rate of HPV-linked cancers is unclear, although some think that it could be
because of changes in sexual practices in recent decades, in particular an increase in oral
sex.
People with oral and oropharyngeal cancer linked with HPV infection tend to be younger
and are less likely to be smokers and drinkers.
Oropharyngeal cancers that contain HPV DNA tend to have a better outlook than those
without HPV.
Gender
Oral and oropharyngeal cancers are about twice as common in men as in women. This
might be because men have been more likely to use tobacco and alcohol in the past. This is
changing, but the recent rise in HPV-linked cancers has been mainly among younger men,
so it is still likely to occur more often in men in the near future.
Age
Cancers of the oral cavity and oropharynx usually take many years to develop, so they are
not common in young people. Most patients with these cancers are older than 55 when the
cancers are first found. But this may be changing as HPV-linked cancers become more
common. People with cancers linked to HPV infection tend to be younger.

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Ultraviolet (UV) light
Sunlight is the main source of UV light for most people. Cancers of the lip are more common
in people who have outdoor jobs where they are exposed to sunlight for long periods of
time.
Poornutrition
Several studies have found that a diet low in fruits and vegetables is linked with an
increased risk of cancers of the oral cavity and oropharynx.
Weakened immune system
Oral cavity and oropharyngeal cancers are more common in people who have a weak
immune system. A weak immune system can be caused by certain diseases present at birth,
the acquired immunodeficiency syndrome (AIDS), and certain medicines (such as those
given after organ transplants).
Graft-versus-host disease
Graft-versus-host disease (GVHD) is a condition that sometimes occurs after a stem cell
transplant. During this medical procedure, blood stem cells from a donor are used to
replace bone marrow that has been destroyed by disease, chemotherapy, or radiation.
GVHD occurs when the donor stem cells recognize the patient’s cells as foreign and launch
an attack against them. GVHD can affect many tissues of the body, including those in the
mouth. This increases the risk of oral cancer, which can occur as early as 2 years after
GVHD.
Genetic syndromes
People with certain syndromes caused by inherited defects (mutations) in certain genes
have a very high risk of mouth and throat cancer.
 Fanconi anemia is a condition that can be caused by inherited defects in several
genes that contribute to repair of DNA. People with this syndrome often have blood

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problems at an early age, which may lead to leukemia or aplastic anemia. They also
have a very high risk of cancer of the mouth and throat.
 Dyskeratosis congenita is a genetic syndrome that can cause aplastic anemia, skin
rashes, and abnormal fingernails and toenails. People with this syndrome also have
a very high risk of developing cancer of the mouth and throat at an early age.
Lichen planus
This disease occurs mainly in middle-aged people. Most often it affects the skin (usually as
an itchy rash), but it sometimes affects the lining of the mouth and throat, appearing as
small white lines or spots. A severe case may slightly increase the risk of oral cancer.
Unproven orcontroversial risk factors
Mouthwash
Some studies have suggested that mouthwash with a high alcohol content might be linked
to a higher risk of oral and oropharyngeal cancers. But recent research has questioned
these results. Studying this possible link is complicated by the fact that smokers and
frequent drinkers (who already have an increased risk of these cancers) are more likely to
use mouthwash than people who neither smoke nor drink.
Irritation from dentures
It has been suggested that long-term irritation of the lining of the mouth caused by poorly
fitting dentures is a risk factor for oral cancer. But many studies have found no increased
risk in denture wearers overall.
Poorly fitting dentures can tend to trap agents that have been proven to cause oral cancer,
such as alcohol and tobacco particles, so denture wearers should have them checked by a
dentist regularly to ensure a good fit. All denture wearers should remove their dentures at
night and clean and rinse them thoroughly every day.

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Etiology
Tobacco and alcohol use are independent risk factors for mouth cancer and tongue cancer.
Heavy tobacco smokers have a 20-fold greater risk; heavy alcohol drinkers a 5-fold greater
risk and those who do both have a 50-fold greater risk. Betel-quid chewing and oral snuff
are important risk factors in people from specific geographic areas (eg, betel chewing in
Southeast Asia). Finally, a diet low in fresh vegetables and fruits has also been implicated in
causing oral squamous cell carcinoma (OSCC), and human papillomaviruses have been
implicated in oropharyngeal cancers.
1) Cigarette smoking: Compared with persons who do not smoke, the risk of oral
cancer in persons who smoke low/medium-tar cigarettes and high-tar cigarettes
was 8.5- and 16.4-fold greater, respectively. (Note that cigarettes are classified as
low/medium if the tar yield is less than 22 mg and high tar if the tar yield is greater
than 22 mg). Note the image below.
Early oral squamous cell carcinoma in the buccal mucosa arising from a chronic candidal leukoplakia
in a person who smokes heavily. The lesion was a painless, chronic indurated lump.
2) Alcohol: Growing evidence is associating increased alcohol consumption with the
risk of developing OSCC. Alcoholic beverages may contain carcinogens or
procarcinogens, including nitrosamine and urethane contaminants and ethanol.
Ethanol is metabolized by alcohol dehydrogenase and, to some extent, by
cytochrome P450 to acetaldehyde, which may be carcinogenic. The combined effects
of tobacco use and alcohol consumption are found to be multiplicative. Compared
with persons who do not drink and do not smoke, the risk of developing OSCC is
increased 80-fold in persons with the highest levels of smoking and alcohol
consumption.
3) Betel and similar habits : The betel quid contains a variety of ingredients, including
betel vine leaf, betel (areca) nut, catechu, and, often, slaked lime together with
tobacco. Some persons chew the nut only, and others prefer paan, which includes
tobacco and sometimes lime and catechu. In 1986, the International Agency for
Research on Cancer has deemed betel-quid chewing an important risk factor, and
the areca (betel) nut habit with or without tobacco use can cause cytogenetic
changes in oral epithelium. Various other chewing habits, usually combinations that

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contain tobacco, are used in different cultures (eg, Qat, Shammah, Toombak).
Tobacco chewing in people from parts of Asia appears to predispose to OSCC,
particularly when it is started early in life and is used frequently and for prolonged
periods. Studies from India have confirmed the association between paan tobacco
chewing and OSCC, particularly cancer of the buccal and labial mucosa.
4) Diet: A significant protective effect of diet against oral cancer has generally been
shown in persons who consume beta-carotene–rich vegetables and citric fruits.
5) Oral health: A case-control study (ie, every oral cancer case prior to surgery and
every control at the time of interview had a structured oral examination) from China
found that wearing dentures, per se, is not a risk factor, although the risk was
increased in men who wore dentures made from metal. Poor dentition, as reflected
by missing teeth, emerged as a strong risk factor independent of other established
risk factors.
6) Mouthwash use: The effect of the alcohol in mouthwash appears to be similar to that
of alcohol used for drinking, although the contribution of mouthwash use to oral
cancer must be small in terms of attributable risk. This controversy continues.
7) Socioeconomic status: Behaviors that lead to social instability or social instability
itself have been linked to an increased risk of oral cancer, but many other
explanations may exist (eg, habits, oral health, diet, nutrition).
8) Infective agents: Candida albicans and viruses, such as herpes viruses and
papillomaviruses, may be implicated in some cases. Human papillomaviruses are
particularly implicated in oropharyngeal cancers. HPV-related tumors tend to be
seen in younger patients, in the fauces, and have usually a better prognosis.
9) Others: Associations also are apparent between oral cancer and other various oral
conditions (eg, oral submucous fibrosis, oral lichen planus, lupus erythematosus,
dyskeratosis congenita, Fanconi anemia).

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Pathogenesis
In oral squamous cell carcinoma (OSCC), modern DNA technology, especially allelic
imbalance (loss of heterozygosity) studies, have identified chromosomal changes
suggestive of the involvement of tumor suppressor genes (TSGs), particularly in
chromosomes 3, 9, 11, and 17. Functional TSGs seem to assist growth control, while their
mutation can unbridle these control mechanisms.
The regions most commonly identified thus far have included some on the short arm of
chromosome 3, a TSG termed P16 on chromosome 9, and the TSG termed TP53 on
chromosome 17, but multiple other genes are being discovered.
As well as damage to TSGs, cancer may also involve damage to other genes involved in
growth control, mainly those involved in cell signaling (oncogenes), especially some on
chromosome 11 (PRAD1 in particular) and chromosome 17 (Harvey ras [H-ras]). Changes
in these and other oncogenes can disrupt cell growth control, ultimately leading to the
uncontrolled growth of cancer. H-ras was one of the oncogenes that first caught the
attention of molecular biologists interested in cell signaling, cell growth control, and
cancer. It and the gene for epidermal growth factor receptor (EGFR) are involved in cell
signaling.
The genetic aberrations involve, in order of decreasing frequency, chromosomes 9, 3, 17,
13, and 11 in particular, and probably other chromosomes, and involve inactivated TSGs,
especially P16, and TP53 and overexpressed oncogenes, especially PRAD1.
The molecular changes found in OSCC from Western countries (eg, United Kingdom, United
States, Australia), particularly TP53 mutations, are infrequent in Eastern countries (eg,
India, Southeast Asia), where the involvement of ras oncogenes is more common,
suggesting genetic differences that might be involved in explaining the susceptibility of
certain groups to OSCC.

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The rare Li-Fraumeni syndrome is associated with defects in TP53.
Carcinogen-metabolizing enzymes are implicated in some patients. Alcohol dehydrogenase
oxidizes ethanol to acetaldehyde, which is cytotoxic and results in the production of free
radicals and DNA hydroxylated bases; alcohol dehydrogenase type 3 genotypes appear
predisposed to OSCC. Cytochrome P450 can activate many environmental procarcinogens.
Ethanol is also metabolized to some extent by cytochrome P450 IIEI (CYP2E1) to
acetaldehyde. Mutations in some TSGs may be related to cytochrome P450 genotypes and
predispose to OSCC. Glutathione S transferase (GST) genotypes may have impaired activity;
for example, the null genotype of GSTM1 has a decreased capacity to detoxify tobacco
carcinogens. Some GSTM1 and GSTP1 polymorphic genotypes and GSTM1 and GSTT1 null
genotypes have been shown to predispose to OSCC. N -acetyltransferases NAT1 and NAT2
acetylate procarcinogens. N -acetyl transferase NAT1*10 genotypes may be a genetic
determinant of OSCC, at least in some populations.
Tobacco is a potent risk factor for oral cancer. An interaction occurs between redox-active
metals in saliva and the low reactive free radicals in cigarette smoke. The result may be
that saliva loses its antioxidant capacity and instead becomes a potent pro-oxidant
milieu. [3]
DNA repair genes are clearly involved in the pathogenesis of some rare cancers, such as
those that occur in association with xeroderma pigmentosum, but, more recently, evidence
of defective DNA repair has also been found to underlie some OSCCs.
Immune defects may predispose to OSCC, especially lip cancer. OSCC is also now being
reported with increased frequency in association with diabetes and systemic sclerosis.
Intraoral OSCC primarily affects the posterior lateral part of the tongue. Spread is local,
especially through muscle and bone, and metastasis initially is to the anterior cervical
lymph nodes and later to the liver and skeleton.

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Clinic
Main Signs & Symptoms
1) Unhealing oral sores
2) Persistent oral pain
3) Lump / thickened cheek
4) White / red patch in oral mucosa
5) Sorethroat ( Foreign body sensation)
6) Dysphagia
7) Difficulty chewing
8) Trismus
9) Difficulty moving Jaw / tongue
10) Tongues / mouth numbness
11) Jaw swelling (Ill fitting dentures)
12) Loose teeth
13) Pain around teeth / gums
14) Lump in mouth
15) Halitosis
16) Voice changes
17) Weightloss
History
Some oral squamous cell carcinomas (OSCCs) arise in apparently normal mucosa, but many
are preceded by clinically obvious potentially malignant disorders (PMDs), especially
erythroplakia (red patch), leukoplakia (white patch), a speckled leukoplakia (red and
white patch), or verrucous leukoplakia, and many others are associated with such lesions
(especially in Southeast Asia). The challenges in predicting which oral mucosal PMD will
progress to neoplasia are discussed more fully elsewhere. [6]
Erythroplastic lesions are velvety red plaques, which in at least 85% of cases, show frank
malignancy or severe dysplasia. In contrast, most white lesions are not malignant or
premalignant. Speckled or verrucous leukoplakias are more likely to be premalignant.
Carcinomas are seen 17 times more frequently in erythroplakias than in leukoplakias, but
leukoplakias are far more common. The prevalence of malignant transformation in
leukoplakias ranges from 3-33% over 10 years; homogeneous leukoplakias are only very
occasionally premalignant, but speckled or verrucous leukoplakias are more likely to be
premalignant.

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In most cases, a biopsy and a histologic examination are required because dysplasia may
precede malignant changes. The rate of malignant changes can be as high as 36% when
moderate or severe dysplasia is present. Be aware that single ulcers, lumps, red patches, or
white patches (particularly if they persist >3 wk) may be manifestations of malignancy.
OSCC may manifest as the following:
 A red lesion (erythroplakia)
 A granular ulcer with fissuring or raised exophytic margins
 A white or mixed white and red lesion
 A lump sometimes with abnormal supplying blood vessels
 An indurated lump/ulcer (ie, a firm infiltration beneath the mucosa)
 A nonhealing extraction socket
 A lesion fixed to deeper tissues or to overlying skin or mucosa
 Cervical lymph node enlargement, especially if hardness is present in a lymph node or
fixation: Enlarged nodes in a patient with oral carcinoma may be caused by infection,
reactive hyperplasia secondary to the tumor, or metastatic disease. Occasionally, a
lymph node is detected in the absence of any obvious primary tumor. Nodal
enlargement is a feature particularly in oropharyngeal cancers.
These potentially malignant disorders and OSCC should be detected at an early stage;
however, many oral tumors still are seen only when advanced. Diagnosis is often delayed
by up to 6 months, even in developed countries, despite exhortations over the past 25 years
to increase the index of suspicion. Early detection and treatment is the short-term goal
because this results in considerably better survival rates. Early carcinomas may not be
painful; however, later, they may cause pain and difficulty with speech and swallowing.
Dental practitioners and dental care professionals should remain vigilant for signs of PMD
and oral cancer whilst performing routine oral examinations.
Physical
A systematic and thorough examination of the mouth, fauces, and cervical lymph nodes
should be performed by a clinician trained in the diagnosis of oral diseases, and a general
physical examination is indicated. Dental practitioners and dental care professionals are
trained in the examination of the mouth.
Advanced caries, periodontal disease, or periapical lesions may need early attention,
especially if radiotherapy is to be used in management of a tumor. Examine the teeth,
periodontium, and entire mucosa in good lighting.
The most common sites of oral cancer include the lower lip, the lateral margin of the
tongue, and the floor of the mouth; however, all areas should be scrutinized. The sump area
or "coffin corner" at the posterior tongue/floor of the mouth is a common site for cancer
but may be missed by cursory inspection; special care is needed to ensure close
examination.

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The clinical appearance of oral cancer is highly variable and includes ulcers, red or white
areas, lumps, or fissures. Lesions always must be palpated after inspection to detect
induration and fixation to deeper tissues.
Erythroplasia (erythroplakia) is a red and often velvety lesion, which, unlike leukoplakias,
does not form a plaque but is level with or depressed below the surrounding mucosa. Of
erythroplasia lesions, 75-90% prove to be carcinoma or carcinoma in situ or show severe
dysplasia. Erythroplasia affects patients of either sex in their sixth and seventh decades and
typically involves the floor of the mouth, the ventrum of the tongue, or the soft palate. Red
oral lesions usually are more dangerous than white oral lesions.
Oral mucosal white patches usually result from increased keratinization or candidosis.
Currently, the term leukoplakia is usually restricted to white patches for which a cause
cannot be established; therefore, the term implies a diagnosis by exclusion (eg, lichen
planus, candidiasis). The term leukoplakia is also used irrespective of the presence or
absence of epithelial dysplasia. Leukoplakia is a clinical term for a persistent adherent
white patch with no histologic connotation and no implied premalignant potential;
keratosis is the term now commonly used. Oral carcinoma can also appear as a white patch.
Most lip cancers manifest on the lower lip at the mucocutaneous junction as a chronic small
lump, ulcer, or scabbed lesion.
Most intraoral cancers manifest on the middle third of the lateral margins of the tongue
with an erythroplastic component and, sometimes, induration.
Late tongue cancer may manifest as an exophytic lesion, an ulcer, or an area of superficial
ulceration with induration.
A typical malignant ulcer is hard with heaped-up and often everted or rolled edges and a
granular floor.
The floor of the mouth is the second most common intraoral site for cancer and more
commonly is associated with leukoplakia. Most cancer arises in the anterior floor of the
mouth as an indurated mass that soon ulcerates, resulting in slurring of speech.
Carcinomas of the alveolus or gingiva are mostly seen in the mandibular premolar and
molar regions, usually as a lump (epulis) or ulcer. The underlying alveolar bone is invaded
in 50% of cases, even in the absence of radiographic changes, and adjacent teeth may be
loose.
Carcinomas of the buccal mucosa are mostly seen at the commissure or in the retromolar
area. Most are ulcerated lumps, and some arise in candidal leukoplakias.
Any single lesion that persists more than 3 weeks, especially if Red, Ulcerated, or a Lump,
Especially with induration (ie, the RULE mnemonic) should be regarded with suspicion and
a histopathological diagnosis established.

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Second primary tumors (SPTs) are additional primary carcinomas (synchronous tumors)
present in as many as 10-15% of persons with oral carcinoma and are most commonly
seen in the mouth in patients with gingival, floor of mouth, lingual, or buccal carcinoma.
SPTs may also be present elsewhere in the upper aerodigestive tract.
Lymph node examination is of paramount importance, and general examination and,
possibly, endoscopy, may be indicated to detect metastases or SPTs. From 30-80% of
patients with oral cancer have metastases in the cervical lymph nodes at presentation. Oral
cancer predominantly metastasizes locally and to regional lymph nodes, primarily in the
anterior neck. Later, dissemination to the lungs, liver, or bones may occur.
Any chronic oral lesion should be regarded with suspicion, especially when found in an
older patient, when lesions appear (see History), with induration, with fixation to
underlying tissues, with any recent changes in appearance, with associated
lymphadenopathy, or with no obvious explanation for the lesion. Examine the entire
mucosa because widespread dysplastic mucosa (field change) or a second neoplasm (see
Staging) may be present. Carefully record the location of suspicious lesions, preferably on a
standard topographic diagram.
Treatment
The choice of treatment depends on
 cell type and degree of differentiation
 site, size, and location of the primary lesion
 lymph node status

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 presence of bone involvement
 ability to achieve adequate surgical margins
 ability to preserve speech
 ability to preserve swallowing function
 physical and mental status of the patient
 assessment of the potential complications of each therapy
 the experience of the surgeon and radiotherapist
 Personal preferences and cooperation of the patient.
T1N0, T2N0 Surgery ± RT
RT -External Beam
-Brachytherapy
T3N0, T4N0 Surgery and Post op RT
N+ ±Chemotherapy
T4b, N3, M+ Pallition
- Primarily RT ±Chemo
(1) Surgery
Surgery may be the primary treatment or may be part of combined treatment with
radiation therapy.
Indications
 Tumors involving bone
 When the side effects of surgery are expected to be less significant than those
associated with radiation
 Tumors that lack sensitivity to radiation

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 Recurrent tumor in areas that have previously received a maximum dose of
radiotherapy
 In palliative cases to reduce the bulk of the tumor
 clinically positive cervical nodes - treatment of choice
Advantages
 Short time – compliance
 Specimen available for HPE
 Helps in planning adjuvant treatment
 No radiation sequelae
Disadvantages
 Tissue & functional loss
 Disfigurement
 Infection
 Bleeding
 Mortality
(2) Radiation
 Curative
 As part of a combined radiation-surgery and/or chemotherapy
 Palliative
Rationale
 Radiation kills cells by interaction with water molecules in the cells
 DNA is disrupted, and chromosomal damage occurs.
 The affected cells may die or remain incapable of division.
 Due to a greater potential for cell repair in normal tissue than in malignant cells and
a greater susceptibility to radiation due to the higher growth fraction of cancer cells,
a differential effect is achieved.
 Radiation therapy is delivered in daily fractions for a planned number of days.
 1.8 – 2 Gy per day (Total 45 – 60 Gy)

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 The relatively hypoxic central tumor cells are less susceptible to radiotherapy, but
they may become better oxygenated as peripheral cells are affected by radiation and
are thus more susceptible to subsequent fractions of radiation
 Less long term complications
 SCCs are usually radiosensitive, and early lesions are highly curable.
 The more differentiated the tumor, the less rapid will be the response to
radiotherapy.
 Exophytic and well-oxygenated tumors are more radiosensitive whereas large
invasive tumors with small growth fractions are less responsive.
 SCC that is limited to the mucosa is highly curable with radiotherapy; however,
tumor spread to bone reduces the probability of cure with radiation alone.
 Small cervical metastases may be controlled with radiation therapy alone
 The radiation treatment plan is determined by tumor site, tumor size, the total
volume to be radiated, the number of treatment fractions, the total number of days
of treatment, and the tolerance of the patient.
 Treatment planning in radiation therapy includes planning for the sparing of
uninvolved tissues or organs.
 The dose to the eye or spinal cord, salivary glands, alveolar bone, and soft tissue can
be limited through the selection of the radiation source, field set-up, and shielding
and by moving the uninvolved tissue out of the field.
Types of Radiation:
1. External beam RT
(a) Telecobalt
(b)Linear accelerator
2. Brachytherapy
(a) Intracavitary - Ca Nasopharynx
(b)Interstitial - Ca Cheek, Tongue
(c) Mould therapy - Ca Palate
3. Internal Therapy
- Ca Thyroid
Advantages of Brachytherapy

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 Well defined volume treated
 Highly localized
 Minimal normal tissue complication
 Short treatment time
Disadvantages
 Invasive
 Need expertise
(3) Palliative
 Pain
 Bleeding
 Fungation
Advantages
 No tissue or functional loss
 No mortality
 Regional nodes can be treated with less morbidity
 Treatment of multiple primary possible
 Better surgical salvage possible with failure
Disadvantages
 Infrastructure
 Treatment is protracted
 Radiation sequelae

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(4) Chemotherapy
Curative
- Neoadjuvant (Induction)
- Adjuvant
- Concurrent: to treat micromets
Palliative
- Recurrence
- Metastatic disease
Drugs - Cisplatin, Methotrexate, 5 FU
Complications-
i. Acute reactions (short term complications) occur during the course of
radiotherapy because of direct tissue toxicity and possibly secondary
bacterial irritation resulting in ‘ulcerative mucositis’.
ii. Chronic complications or late radiation reactions occur due to change
in the vascular supply, fibrosis in connective tissue and muscle, and
change in the cellularity of tissues. These complications develop slowly
over months to years following treatment.
iii. Hyperfractionation of radiation therapy may reduce the late
complications but may increase the severity of the acute reactions.
Complication prevention:
Pretreatment oral and dental assessment:
1.Reduce the risk or severity of complications
2.Reduce the risk of infection involving the dentition and mucosa
3.Minimize and manage the complications of hyposalivation.
Directed at maintenance of:
 Mucosal and bony integrity

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 Dental and periodontal health
 Salivary gland function
 Prevention of potential complications of therapy.
Treatment planning:
 The radiation treatment plan is determined by tumor site, tumor size, the total
volume to be radiated, the number of treatment fractions, the total number of days
of treatment, and the tolerance of the patient.
 Treatment planning in radiation therapy includes planning for the sparing of
uninvolved tissues or organs.
 The dose to the eye or spinal cord, salivary glands, alveolar bone, and soft tissue can
be limited through the selection of the radiation source, field set-up, and shielding
and by moving the uninvolved tissue out of the field.
Prevention
Avoid risk factors
Not all cases of oral cavity and oropharyngeal cancer can be prevented, but the risk of
developing these cancers can be greatly reduced by avoiding certain risk factors.
Limit smokingand drinking
Tobacco and alcohol are among the most important risk factors for these cancers. Not
starting to smoke is the best way to limit the risk of getting these cancers. Quitting tobacco
also greatly lowers your risk of developing these cancers, even after many years of use. The
same is true of heavy drinking. Limit how much alcohol you drink, if you drink at all.
Avoid HPV infection
The risk of infection of the mouth and throat with the human papilloma virus (HPV) is
increased in those who have oral sex and multiple sex partners. These infections are also
more common in smokers, which may be because the smoke damages their immune
system or the cells that line the oral cavity. These infections are common and rarely cause
symptoms. Although HPV infection is linked to oropharyngeal cancer, most people with

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HPV infections of the mouth and throat do not go on to develop this cancer. In addition,
many oral and oropharyngeal cancers are not related to HPV infection.
In recent years, vaccines that reduce the risk of infection with certain types of HPV have
become available. These vaccines were originally meant to lower the risk of cervical cancer,
but they have been shown to lower the risk of other cancers linked to HPV as well, such as
cancers of the anus, vulva, and vagina. HPV vaccination may also lower the risk of mouth
and throat cancers, but this has not yet been proven.
Since these vaccines are only effective if given before someone is infected with HPV, they
are given when a person is young, before they are likely to become sexually active.
For more information see our document HPV Vaccines.
Limit exposure to ultraviolet (UV) light
Ultraviolet radiation is an important and avoidable risk factor for cancer of the lips, as well
as for skin cancer. If possible, limit the time you spend outdoors during the middle of the
day, when the sun’s UV rays are strongest. If you are out in the sun, wear a wide-brimmed
hat and use sunscreen and lip balm with a sun protection factor (SPF) of at least 15.
Eat a healthy diet
A poor diet has been linked to oral cavity and oropharyngeal cancers, although it’s not
exactly clear what substances in healthy foods might be responsible for reducing the risk of
these cancers.
In general, eating a healthy diet is much better than adding vitamin supplements to an
otherwise unhealthy diet. The American Cancer Society recommends eating a healthy diet
that emphasizes plant foods. This includes eating at least 2½ cups of vegetables and fruits
every day. Choosing whole-grain breads, pastas, and cereals instead of refined grains, and
eating fish, poultry, or beans instead of processed meat and red meat may also help lower
your risk of cancer.

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Wearproperly fitted dentures
Avoiding sources of oral irritation (such as dentures that don’t fit properly) may also lower
your risk for oral cancer.
Treat pre-cancerous growths
Areas of leukoplakia or erythroplakia in the mouth sometimes progress to cancer. Doctors
often remove these areas, especially if a biopsy shows they contain areas of dysplasia
(abnormal growth) when looked at under a microscope.
But removing areas of leukoplakia or erythroplakia does not always prevent someone from
getting oral cavity cancer. Studies have found that even when these areas are completely
removed, people with certain types of erythroplakia and leukoplakia still have a higher
chance of developing a cancer in some other area of their mouth.
This may be because the whole lining of the mouth has probably been exposed to the same
cancer-causing agents that led to these pre-cancers (like tobacco). This means that the
entire area may already have early changes that can lead to cancer. This concept is
called field cancerization.
It is important for patients who have had these areas removed to continue having checkups
to look for cancer, and for new areas of leukoplakia or erythroplakia.
Chemoprevention
In recent years, doctors have been testing medicines to try to help lower the risk of these
cancers. This approach, called chemoprevention, is particularly needed for people who
have a higher risk of these cancers, such as those with leukoplakia or erythroplakia.

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Several kinds of drugs have been studied for oropharyngeal cancer chemoprevention, but
most of the research has focused on drugs related to vitamin A (retinoids). Studies so far
have shown that retinoids can cause some areas of leukoplakia to shrink or even go away
temporarily. But these studies have not found a long-term benefit in preventing cancer or
helping patients live longer. At the same time, most of these drugs have bothersome and
even serious side effects.