Oral Cancer

Introduction
1
• The term “oral cancer” includes cancer of the lip, cancer of the tongue and
cancer of the mouth. There can be no doubt that cancer of the oral cavity is a
major health problem throughout the world. A remarkable feature of cancer is
its unequal distribution worldwide. For instance, in respect to cancer of the lip,
the highest and lowest age-adjusted incidence rates in males were found
respectively in Newfoundland and Jews born in Africa (Muir and Peron 1976).
The tumour is, however, uncommon in Africans (Edington and Sheihan 1966;
Oluwasanmi et al. 1969, Templeton 1973). In many areas of Asia, oral cancer
is the commonest malignant disease, accounting for 40% of all cancers. In
Northern Nigeria and among the Yorubas and Igbos of Southern Nigeria,
cancer of the oral cavity is not a great problem because the potent
carcinogens concerned with the causation are lacking in these communities
(Edington and Sheihan 1966; Onuigbo 1977; Adekeye, Asamoa and Cohen
1985). Globally, the WHO assesses that oral cancer is the third commonest
malignancy among males and sixth commonest in females. The incidence of
the disease in the so-called “developed” nations is certainly lower than in Asia,
although great variations exist even within Europe with the incidence in Bas-
Rhin (France) exceeding that in Bombay (India).
 Introduction 2
• The main aetiological risk factors are recognised as tobacco habits
and a high alcohol intake, with a strong synergistic relationship
between the two, which increases the risk considerably. There are a
number of other risk factors that have been postulated, including
chronic candidal infection, and nutritional deficiencies. The level of
risk with these other factors remains unproven in most cases and is
certainly small compared with tobacco and alcohol. In younger
patients in particular it is often difficult to find any obvious
predisposing factors. There are also certain well-recognised
premalignant lesions such as erythroplakia, leukoplakia and
arguably erosive lichen planus. The management of these lesions is
a matter for debate. The increased risk is difficult to quantify but
factors such as site, histology and length of time the lesion has been
present are all important
 Introduction 3
• Oral cancer is still a lethal disease, with a 5-year survival
of less than 50%. The annual mortality figures are
actually of the same order of magnitude as malignant
melanoma or cervical cancer, both of which are subject
to intense media interest, educational campaigns and
screening programmes. It is therefore interesting to ask
why there appears to be less interest in oral cancer
despite the emotional, functional and aesthetic
importance of the face and mouth. Unfortunately, many
patients, especially in Nigeria, still present with advanced
disease (Oji 1999). The importance of patient education
and regular screening by dentists and doctors needs to
be emphasised. The message to all health professionals
must be “If in doubt refer early”.
 Applied Anatomy
1
• The oral cavity is divided into the following anatomical sites (Fig.1)
which are quite distinct from the “oropharynx”:
  lips
  buccal mucosa
  retromolar trigone
  anterior two-thirds of tongue
  floor of mouth
  gingivae (or alveolar ridge in the absence of teeth)
  hard palate
• The oral cavity is lined by mucous membrane which may be:
  lining, e.g. floor of mouth
  functional, e.g. palate
  specialised, e.g. tongue dorsum
 Applied Anatomy 2
• Histologically the mucous membrane is
composed of stratified squamous epithelium,
which, unlike skin, is normally non-keratinising,
does not contain a stratum lucidum, and has
quite a rich neural and vascular supply. This
renders oral mucosa relatively more sensitive
than skin, with a greater healing potential.
• The oral mucosa is more susceptible to
environmental carcinogenic agents than skin,
because of its greater permeability, although
saliva plays a more protective role.
Applied Anatomy 3
 Oral Function
1
• The mouth serves the following important
functions:
  mastication and swallowing
  speech
  facial and emotional expression
 Oral Function 2
• Oral cancer will compromise the above features
therefore, subsequent treatment should ideally
aim to restore lost function. In reality, however,
cancer treatment tends to exacerbate the
problem of compromised function; hence
rehabilitation plays just as much a role in the
overall management of the cancer patient, as
does the cure. For example, a patient who is
cured of cancer but as result of the treatment will
never be able to eat, speak, or look normal
again has a reduced quality of life and cannot be
considered a complete success.
 Epidemiology of Oral Cancer

• Epidemiology is the basis from which

disease prevention strategies are
formulated
 Descriptive epidemiology
• Descriptive epidemiology describes the
patterns of disease occurrence in
populations. That is, it examines the extent
of the oral cancer problem in terms of
numbers of cases; time trends; geographic
distributions; rates of incidence or mortality
in different population groups.
 Analytical epidemiology
• Analytical epidemiology examines the
aetiological relationships of oral cancer, hence it
focuses on: causes of oral cancer; determinates
of the progression of oral cancer
• Occurrence of disease in a live population
• The incidence equals the number of new cases
and the prevalence is the number of current
cases.
 Worldwide distribution
• Worldwide the incidence of oral cancer varies enormously. The
highest reported rates are in India and Sri Lanka where oral cancers
are often the commonest site for malignancy, sometimes causing
over 40% of all cancers compared to around 1% in the UK. Other
areas of high incidence outside Europe include Papua New Guinea
and parts of South America such as Brazil.
• Generally the highest rates of oral cancer are found in the
developing world where oral cancer and pharynx combined is the
third commonest site of cancer: globally there are about 378,500
new cases each year. However, there are pockets of high incidence
in Western countries such as Bas-Rhin in France and
Newfoundland (lip only) in Canada. In addition, in many Western
European countries the rates have increased in recent decades.
 Age distribution
• The incidence of oral cancer increases
with age and in Britain the majority of
cases (85%) occur in people aged over 50
years. However, in high prevalence areas
in the developing world, it is relatively
common in younger people and the
teenage use of oral snuff in the USA has
been linked to oral cancer appearing in the
third and fourth decades of life.
 Sex distribution
• In most countries the disease has always been
commoner in men than in women but the sex
ratio has decreased as male rates have fallen
proportionately more than female rates. Fifty
years ago oral cancer caused five times more
death in men than in women, but now the
mortality ratio is less than two to one. In certain
high risk areas in South Asia female rates are
sometimes as high as or higher than the male
rates.
 Trends
• 90 years ago cancer of the lip and tongue alone caused over 1200
deaths each year in England and Wales compared to 400 today.
However, in recent years the incidence and mortality rates have
started to increase for cancer of the tongue and mouth, especially in
younger men. Analyses of these trends suggest that there is a
strong cohort effect, with men born after 1910 having higher rates
(Osmond et al 1983). In North America the increase in tongue
cancer has been linked to the growth in smokeless tobacco
consumption (Davis and Severson 1987). Increases in mortality
from cancer of the oral cavity and pharynx over the past 20-30 years
have also been reported for almost all the EU countries. Unless
such increases seen in younger cohorts in many countries are
halted or reversed, they will inevitably lead to higher overall rates as
these populations age, making oral cancer a more important health
problem in the future.
 Incidence of malignant tumours
of the oral cavity
• Squamous cell carcinoma 90%
• Adenocarcinoma (salivary gland tumours) 8%
• Sarcomas 2%
• Frequency by oral site
• Lower lip 30%
• Tongue 20%
• Floor of mouth 15%
• Mandibular alveolus 15%
• Buccal mucosa 10%
• Maxillary alveolus and palate 10%
• Moore and Catlin in 1967 stated that 75% of all squamous cell
carcinomas were found in an area that represented less than 20%
of the oral mucosa. This includes the lingual surface of the alveolus,
the floor of mouth and the ventral surface of the tongue (the “sump”
areas).
 Aetiology 1

• Oral cancer is a multifactorial disease

where no single clearly recognisable
cause has been found. The precise role of
any individual factor or condition is poorly
understood
 Aetiology 2
• Social habits
• Tobacco
• Alcohol
• Areca nut wrapped in betel vine
• Infections
• Bacterial, i.e. tertiary syphilis
• Fungal, i.e. candidal leukoplakia
• Viral, i.e. herpes, papilloma, HIV
• Extrinsic factors
• Actinic radiation (sunshine)
• Industrial hazards, i.e. chemical industry
• Poor oral hygiene and ill-fitting dentures
• Intrinsic factors
• Genetic, i.e. dyskeratosis congenita
 Tobacco 1
• Tobacco consumption can take many forms and the
primary cause of the very high incidence of oral cancer
in South Asia is the widespread habit of chewing betel
quid to which tobacco is added. An estimated 200 million
people worldwide practice this habit. The longer the quid
is kept in the mouth, the higher the risk and if chewing is
combined with smoking, then the risk is even higher. All
forms of smoking tobacco carry a risk of oral cancer and
particularly high rates occur when reverse smoking
with the lighted end inside the mouth is practised.
Tobacco chewing is more clearly associated with
verrucous carcinoma and leukoplakia
 Reverse chutta smoking is common in some parts of
India, where it is particularly popular amongst women
and carries an even higher risk than betel quid chewing.
 Tobacco 2
• In the Sudan the smokeless tobacco (ST)
product used widely is referred to as
toombak. It is a mixture of tobacco and
sodium bicarbonate. The habit is practised
by placing a quid in the oral vestibule for
periods varying from a few minutes to
several hours. Toombak-associated oral
mucosal lesions in Sudanese show a low
prevalence of epithelial dysplasia.
 Tobacco 3
• In Western countries cigarette, cigar and pipe
smoking are the main forms of of tobacco use. In
the earlier parts of the 20th century, pipe
smoking was associated with lip cancer and its
decline in popularity may be linked with some of
the decrease in lip cancer. However, the main
form of tobacco consumption since 1919 is
cigarette smoking which is a risk factor for oral
and many other cancers, especially lung cancer.
 Tobacco 4
• In the UK inhaling tobacco as snuff, snuff-dipping and
chewing tobacco are rare habits but recently there was
an attempt by the tobacco industry to introduce
smokeless tobacco to the younger generation in the form
of Skoal Bandits. These have now been banned in the
EC. The use of smokeless tobacco has become
common in the USA (an estimated 12 million users in
1985) and has led to an increase in oral lesions in young
people.
•
 Snuff-dripping consists of placing a pinch of snuff
between the gum and cheek or upper lip.
  Skoal Bandits are small paper pouches containing oral
snuff.
 Areca nut in betel vine 1
• Areca nut, often mistakenly referred to as “betel
nut”, and commonly called Supari, is the fruit of
the Areca catechu (L) tree. The areca palm is
native to South Asia and the Pacific islands. The
fruit is green in colour (golden-yellow when ripe)
and the seed or endosperm is consumed fresh,
boiled, after sun drying or curing. The alkaloids
released when the nut is chewed provoke
excessive and abnormal synthesis of collagen
by cultured fibroblasts; hence there is a good
relationship with oral submucous fibrosis (OSF).
 Areca nut in betel vine 2
• It predominantly affects Asiatic people and is
characterised by rigidity of the oral mucosa of
varying intensity due to fibro-elastic
transformation of the juxta-epithelial and deeper
connective tissue. It is a chronic progressive
disease leading to marked limitation of jaw
opening. The poor are at particular risk, because
they are likely to be malnourished, anaemic and
will chew continuously in order to suppress
hunger.
 Areca nut in betel vine 3
• Major components of the betel quid include betel
leaf, areca nut, lime, catechu (a resinous extract
from the Acacia tree) and sometimes tobacco. In
the Karachi community (Pakistan) the term pan
is usually taken to mean betel leaf, areca nut,
lime and condiments without tobacco. Areca nut
is chewed either alone as plain chopped or in
commercially available packet form which
includes sweeteners. Some individuals chew
both pan and areca nut products at different
times of the day.
 Alcohol 1
• Alcohol is the second major risk factor for oral cancer as
well as for cancers of the pharynx, oesophagus, larynx
and liver and it may be an important aetiological factor in
at least three ways:
• Liver damage and secondary nutritional deficiencies, i.e.
B complex vitamins which increase the susceptibility of
oral mucosa to environmental carcinogens.
• Alcohol may directly damage mucosa and make it more
permeable.
• Impurities present in alcoholic beverages may be the real
culprits.
 Alcohol 2
• Alcoholics and other heavy users of alcohol are at much higher risk
and conversely, populations with a low alcohol intake have very low
risk. Alcohol and smoking risks have been shown to be
multiplicative for the mouth, additive for the larynx and in between
multiplicative and additive for the oesophagus, reflecting the likely
local exposure to these agents. In Denmark, the alarming rise in oral
cancers has been attributed predominantly to increased alcohol
consumption. In the UK the Health Education Authority recommends
a safe weekly consumption of not more than 21 units for men and
14 units for women.
• Concern has recently been expressed in the USA about frequent
use of mouthwashes with a high alcohol content. It might be wise to
avoid such use.
•
 1 unit = ½ pint beer = 0,284l beer = 1 single measure of spirit = 1
small glass of wine
 Diet and Nutrition 1
• The protective effects of diets rich in antioxidants
(vitamin A, C and E) and trace elements (Zn, Se
and Cu) are well established (Enweonwu and
Meeks 1995; Winn 1996). Conversely, leanness
is associated with risk of oral cancer (Kabat et al
1994). This has led to an explosion of interest in
the use of natural (e.g. β-carotene and α-
tocopherol) and synthetic (e.g. retinoids)
antioxidants in chemoprevention, the
management of premalignant lesions and in the
prevention of second primary neoplasm.
 Diet and Nutrition 2
• Patients with chronic iron deficiency such as Plummer-
Vinson syndrome develop gastrointestinal mucosal
atrophy, including that of the oral cavity and have a
higher susceptibility to oesophageal and oral carcinoma.
• There is limited evidence on directly carcinogenic food
components with respect to oral, head and neck cancer
(unlike the rest of the gastrointestinal tract and the
breast), but two recent studies have shown significant
increased risks for heavy and long-term consumption of
nitrite and nitrosamine-containing foods, such as smoked
or slated fish or meats (De Stefani et al 1994; Rogers et
al 1995).
 Viruses
• There is no direct evidence yet, but three possible
mechanisms have been proposed:
• May induce cancer mutations in infected cells by
inserting parts of their own genome into host DNA.
• May upset the growth regulatory activity of certain host
cell genes known as proto-oncogenes.
• May help accelerate cell proliferation.
• Viruses contribute only one step in the multistep process
of malignant transformation, hence additional factors,
such as environmental and genetic factors are required.
 Ultraviolet light. 1
• Light-skinned individuals whose skin does
not tan well and who sustain prolonged
occupational or recreational exposure to
direct sunlight are at a greater risk of
developing squamous cell carcinoma of
the lower lip.
 Ultraviolet light. 2
• Usually the lip goes through a series of preneoplastic
changes that become progressively worse as the dose of
actinic radiation accumulates and the patient ages. The
sharp ridge or line of demarcation on the vermilion
border is replaced by a puffy, rounded margin, and the
skin develops multiple vertical creases. The exposed
mucosal surface becomes mottled, consisting of red
(atrophy) and white (hyperorthokeratosis) patches, and
displays prominent superficial vascular structures
(telangiectasia). This accumulation of changes is termed
actinic cheilitis (also solar cheilosis, solar keratosis, or
solar elastosis) (Fig. 2).
 Ultraviolet light. 3
• As time and exposure continue, recurring chronic ulcers
frequently develop on the lip, lateral to the midline.
Eventually, the ulcers stop healing, at which point biopsy
usually reveals that a superficial well-differentiated
squamous cell carcinoma has formed. Treatment of the
altered tissue before the development of malignancy
usually consists of superficial surgical removal of the
damaged tissue (“lip stripping” or “lip shave”). When
biopsy reveals the presence of invasion, surgical wedge
resection is usually adequate unless metastasis has
occurred.
Ultraviolet light. 4
 Industrial hazards
• Workers in the construction industry have
increased risk of, particularly, oropharyngeal
cancer with relative risks for exposure to cutting
oils, iron dust, asbestos cement, cement and
coal/tar products. Air pollution, from fossil fuel
stoves, is also demonstrably relevant. This and
city pollutions from vehicles and factories need
much more extensive study. Again, however,
reported relative risks are small and there must
be many confounders.
Immunodeficiency/Suppression.
1
• Acquired immunodeficiency syndrome (AIDS)
predisposes relatively young individuals to various oral
and nonoral malignancies. Intraoral squamous cell
carcinoma is among the number of malignant lesions
that occur at a much younger age than normal for this
condition and without the usual associated aetiological
factors (Fig. 3). Oral Kaposi sarcoma and lymphoma,
which also occur at a younger age in AIDS patients are
much more common than squamous cell carcinoma. It is
now clear that organ transplant patients on
immunosuppression regimes have an increased risk of
dysplastic and malignant lip lesions – as with sun-
exposed skin (King et al 1995).
Immunodeficiency/Suppression.
2
 Dentition
• Trauma of the soft tissue resulting from
poor dentition and ill-fitting dentures may
play a role in localising a site where
tumours develop, but both this and oral
sepsis are very unlikely to cause cancer in
the absence of the above mentioned risk
factors.
 Pre-cancer
• Many oral cancers arise de novo and seem to present as
invasive new lesions without the patient or clinician being
aware of any pre-existing changes. However, several
oral lesions and conditions can precede oral carcinoma –
the most common and important of these are,
leukoplakia (white patches) and erythroplakia (red
patches), the latter being potentially more dangerous.
People with these conditions are at a greater risk of
developing oral cancer than normal populations, even
though the rate of malignant transformation is low,
between 2 and 6%.
 Familial and genetic
predisposition
• This is an important question given the
established hereditary nature of a number of
(rare) malignancies such as retinoblastoma,
nephroblastoma (Wilms’ tumour), for example,
and the familial clustering of some forms of
colon and breast cancer. Geographic/ethnic
differences in the prevalence of ras and p53
gene abnormalities in oral cancer and precancer
may, at least in part, be explained by
racial/genetic differences in susceptibility
(Ranasinghe et al 1993).
 Prevention
• Prevention plays an essential part in the
control and reduction of oral cancer within
the general population. There are three
levels of prevention.
 Primary prevention 1
• This is aimed at reducing or eliminating exposure to
carcinogens so as to prevent initiation or promotion of
the basic carcinogenic process. With such known risk
factors as tobacco and alcohol (carrying an estimated
attributable risk close to 75-95%), it is theoretically
possible to prevent a substantial proportion of oral
cancer. The benefits of eliminating tobacco use and
reducing alcohol intake are well documented in Western
countries and would reduce mortality from many cancers
as well as diseases such as ischaemic heart disease.
The European 10-point code advises people to stop
smoking and to drink in moderation.
 Primary prevention 2
• In India and Sri Lanka successful efforts are being made
to reduce the incidence of the traditional habit of betel
chewing. The greatest cost-benefit is gained by
educating children not to take up the chewing habit. One
method of lowering the risk of oral cancer would be to
give dietary supplements or better still to ensure a
balanced diet that would also reduce the risk of other
diseases.
• As ever, primary prevention remains the ideal. However,
inertia, and often, perversity of the human behaviour and
custom transcend time and culture, thus remaining a
formidable obstacle (Oji 1993).
 Secondary prevention 1
• This refers to the establishment of
screening and early detection programmes
that serve to identify early cases, so that
treatment increases the chance of cure.
• My experience in Nigeria has shown that
delay by the patient was the main cause
for late referral
Secondary prevention 2
 Secondary prevention 3
• This indicates the need for more public education about
the signs of oral cancer (see Pre-cancer section). The
dental profession in both developing and developed
countries is uniquely placed to play a key role in the
detection of oral cancer. Information on the early signs of
the disease should be given in their outpatient clinics and
elsewhere. Patients with leukoplakia, erythroplakia and
persistent mouth ulcers should be encouraged to seek
dental (or medical if the former is unavailable) advice.
• Screening programmes are recommended for the early
detection of oral cancer and precancer in high risk areas
of the third world and in high risk groups in Western
countries.
 Tertiary prevention
• This is the treatment of oral cancer, aimed
at curing the disease at an early stage
without undue complications, such as the
spread of the diseases to other sites of the
body.
Clinical predictors of oral cancer
1
• Key Points
• Site: For example: commissure, in bidi
smokers; floor of mouth, in smokers and
drinkers; lateral border of tongue in smokers and
drinkers; cheeks, lower sulci and retromolar
trigone, in chewers.
• Size: Of itself not significant but wide field
changes indicate greater risk
 bidi is smoked in India. It is derived from the
dry leaves of a tree called tendu. These leaves
are rolled in cigarette form and smoked.
Clinical predictors of oral cancer
2
• Shape: Nodular, ulcerated and verrucous lesions carry a
greater risk.
• Shade: Erythroplakia carries a greater risk than mixed
red and white lesions that carry a greater risk than white
lesions.
• Consistency: There are no hard and fast rules.
• Surroundings: Look for widespread atrophy or other
lesions indicating systemic predisposition or field
change.
• Surface: ulceration, smooth lobulation.
– These considerations are also relevant to the diagnosis and
prognosis of overt malignancy, plus: size does not matter, as do
induration, fixation and other measures of extent, including
lymphadenopathy.
 Classification of Oral Tumours

• There are many classifications of oral

tumours, the most universal of which is
that described by the World Health
Organisation. Disease classifications are
constantly changed and updated, so
perhaps the easiest classification is that
which encompasses all diseases under
very broad headings.
 1. Tumours of the mouth (soft
tissue)
• epithelial tumours.
• connective tissue tumours.
• pigmented tumours.
• lymphoreticular tumours.
• granular cell tumours
 2. Tumours of the jaws (hard
tissues)
• stromal – examples: odontogenic and
primary bone tumours.
• haematopoietic – example:
lymphoreticular tumours.
• invasive – examples: tumours arising
from mucosa or salivary glands.
• metastatic – example: adenocarcinomas
originating from kidney, breast, thyroid.
 Oral Squamous Cell Carcinoma
1
• Squamous cell carcinoma (SCC), sometimes termed
epidermal carcinoma, is defined as a malignant
neoplasm derived from or exhibiting the morphologic
features of squamous epithelium. Squamous cell
carcinoma is often the end stage of alteration in stratified
squamous epithelium, beginning as an epithelial
dysplasia and progressing until the dysplastic epithelial
cells breach the basement membrane and invade the
connective tissue. It also may arise de novo from the
overlying stratified squamous epithelium and not have a
prolonged premalignant phase.
 Oral Squamous Cell Carcinoma
2
• Oral malignancies represent 3% of all cancer in
males and 2% in females. The overall survival
rate of patients with oral malignancies is 50%.
They are responsible for 2% of the annual
deaths in males and 1% in females. As stated
earlier, the incidence of oral cancer differs
extensively, depending on the tobacco habits
prevalent in the various countries throughout the
world. The incidence of oral cancer greatly
increases in societies where extensive tobacco
use begins early in life and is continuous.
 Oral Squamous Cell Carcinoma
3
• Squamous cell carcinoma is by far the
most common malignant neoplasm of the
oral cavity, representing approximately
90% of all oral cancers. It will be
considered in further detail throughout this
book. Unless otherwise stated, the
subsequent chapters on treatment and the
term cancer will refer to squamous cell
carcinoma arising from the oral mucosa
 Clinical presentation 1
• 1. Early lesions:
• asymptomatic
• white or red patches
• small exophytic growth
• small indolent ulcer
• 2. Intermediate lesions:
• persistent ulceration
• induration
• fixation to underlying structures
• lymph node enlargement (may be non-specific)
 Clinical presentation 2
• 3. Advanced lesions:
• haemorrhage or necrosis of exophytic
mass
• destructive crater-like ulcer with raised or
rolled edges
• pain, paraesthesia
• bone destruction, invasion, fracture
• mobility of teeth
 Diagnosis

• A diagnosis is a clinical sum total of the

patient’s presenting condition that should
accurately reflect the underlying pathology
and the clinical signs and symptoms of the
disease. The diagnosis of oral cancer is
more meaningful when it is described in
terms of the TNM staging of oral cancer
(Union Internationale Contre le Cancer,
1987; American Joint Committee on
Cancer, 1988).
 Purpose of staging a patient’s
disease
• Staging provides a standard communicable description
of the tumour. It helps in planning of treatment and
assessment of prognosis. Also, it allows comparison of
treatment results between different centres, as well as
different treatment protocols in one centre. The
classification applies to:
• anterior two-thirds of the tongue
• floor of mouth
• buccal mucosa
• alveolar process
• hard palate
 TNM definition
• T = Primary tumour
• T0 = no evidence of primary tumour
• T1S = carcinoma in situ
• T1 = greatest diameter ≤ 2cm
• T2 = greatest diameter > 2cm but ≤ 4cm
• T3 = greatest diameter > 4cm
• T4 = massive tumour > 4cm with deep invasion
• N = lymph node metastasis
• N0 = no regional lymph node metastasis
• N1 = metastasis in a single ipsilateral node ≤ 3cm
• N2A = metastasis in a single ipsilateral node > 3cm ≤ 6cm
• (in its greatest dimension)
• N2B = metastasis in multiple ipsilateral nodes > 6cm
• N2C = metastasis in bilateral or contralateral lymph nodes,
• none < 6cm
• N3 = metastasis in a lymph node > 6cm (in its largest
 Staging of oral cancer
• Stage 0 = T1S, N0, M0
• Stage 1 = T1, N0, M0
• Stage 2 = T2, N0, M0
• Stage 3 = T3, N0, M0, or N1 with T1, T2
or T3
• Stage 4 = T4, N0 or N1, M0
• Any T, N2 or N3, M0
• Any T, any N, M1
 Treatment Planning

• The two main goals of cancer therapy are to achieve a

disease-free physical state of health and an acceptable
quality of life after treatment.
• The treatment of oral cancer involves a multifaceted
approach that comprises a team of specialists each of
whom plays an essential role in the overall care of the
patient. The team approach to cancer management has
a substantial bearing on the potential for a successful
outcome. Multidisciplinary cancer units ensure that
streamlined communications between the various
speciality groups will result in efficient and effective
management and rehabilitation of each patient.
 Treatment modalities
• Surgery
• Radiotherapy
• Chemotherapy
• Lasers, immunotherapy, gene therapy, etc.
• Homeopathy
• Magnetotherapy
• Note: Orthodox medicine maintains that only surgery
and
• radiotherapy are curative.
• Deciding which modality to use is dependent upon the
aim of treatment (i.e. cure or palliation), the stage of the
disease, the health of the patient and functional and
aesthetic requirements
 Prognostic Indicators

• Factors which are of paramount importance in deciding on prognosis are:

• T = size (maximum diameter) of presenting tumour
• N = degree of lymph node involvement
• M = presence or absence of blood-borne metastasis
• S = site, the further posterior the tumour in the
• mouth, the worse the prognosis
• P = histopathological grading of tumour; poor
• differentiation has poor prognosis
• V = velocity of tumour growth
• D = depth of spread or thickness of tumour (more
• precise than “T” rating)
• A/S = age – the young and the very old have a
• poorer prognosis
• sex – males have a poorer prognosis
 Five-year survival
• The overall 5-year survival for all stages of
this disease is 30-40%. The survival rate
for oral cancer can be determined
according to the stage of the disease.
Using the tongue as an example, the 5-
year survival rate for oral cancer can
range from 90% for stage I disease to 64%
for stage II disease and 34% for stage III
disease, down to a very poor 6% for stage
IV or advanced disease.