2. Introduction:
– Oral cancer can be referred to as the cancer present in the oral
cavity in which 90% of these cancers are squamous cell
carcinoma.
– The most common sites of the oral cavity that are prone to
developing oral cancer include:
– The soft tissues of the oral cavity are covered by stratified
squamous epithelium.
– The oral epithelium plays an essential role in the protection of
the underlying tissues against:
– The epithelium is characterized by its continuous cell renewal and
replacement that is achieved through:
Lips
Labial and Buccal
Mucosa
Floor of the Mouth
Soft Palate Tongue
The loss of fluids
The penetration of potentially harmful
environmental agents such as enzymes,
microbial toxins & carcinogens from
foods and beverages
The division of cells present
in the deeper layers
The rapid desquamation of
surface cells
3. – This constant renewal acts as a protective mechanism as it:
– Cell death is a must for the compensation of cell proliferation in
which:
– DNA can be defined as a nucleic acid containing hereditary
information (genetic information) that gives the body cells
instructions for producing proteins necessary for important body
functions.
Limits the invasion and colonization of microorganisms
adherent to the mucosal surfaces
Eliminates malfunctioning and diseased cells
The production of
cells in the deeper
layers
Balanced by cell
desquamation
from the surface
Results in the
maintenance of
the oral mucosa
integrity
4. – Genes are considered to be the basic physical and functional units
of heredity in which all living organisms rely on them for holding
information necessary for maintaining and building their body
cells
Definition of Oral Cancer:
– An imbalance between cell proliferation and apoptosis which is
the programmed cell death results in the development of cancer
in susceptible patients.
– Thus, cancer can be referred to as the uncontrollable growth of
the tissue in these patients.
Transcription involves copying a gene’s DNA sequence when the gene is
active
Contain sequence of nucleotides that are responsible for determining
what the gene does and when the gene is active (expressed)
Make up chromosomes
Are portions of DNA
Genes
5. Incidence:
– Oral cancer accounts for about:
– The causes of these differences include:
Age, sex & race:
– An increase in age is associated with an increase in the risk of
intraoral cancer as with so many carcinomas suggesting that
any carcinogen have to act over a prolonged period of time.
Overall male to female
ratio
3:1
•White men are associated with the higher risk of
developing intraoral cancer than do any other group
After 65 Years of Age
•Males tend to have a much higher incidence of intraoral
cancer than females
At All Age Levels
40% in
India,
Srilanka
, Sudan
1-2% In the
United
Kingdom
5% In
the
United
States
Different population
habits such as the
tobacco or snuff
chewing habit which is
considered to be
widely spread (40%)
Inadequate education
for the prevention of
oral cancer
The quality of medical
records in different
countries
6. Oral cancer: A Genetic Disease
– Cancer forms when genes within a normal cell are damaged and
mutated.
– Mutations occur in certain key genes which can be grouped into
three classes:
Proto-Oncogenes:
•These are growth promoting genes
•They are normal genes that aid in the regulation of cell
differentiation and growth
•Their normal function is to give instructions to cells about when
to grow and divide
Tumor Suppressor Genes {Anti-Oncogenes}:
•These are growth inhibition genes
•They play a major role in the protection of cells from being one
step on the path to cancer
•Their normal function is to maintain cells in a non-dividing state
DNA Repair Genes:
•Their normal function is to repair damage to DNA
Key Genes
Proto-Oncogenes
Tumor Suppressor
Genes {Anti-
Oncogenes}
DNA Repair
Genes
7. – Mutations may result in the transformation of a proto-oncogene
into activated oncogene by the action of:
– The activation of oncogenes results in the stimulation of the
production of new genetic material in excessive amounts.
– Oncogenes are genes that play a vital role in the onset and
development of cancer.
– How key genes become defective?
It is considered difficult to address the answer of this
question
Chemical
Carcinogens
Irradiation Viruses
The cell can progress to cancer
This causes a loss or reduction in the gene's function
It becomes inactive
When a tumor suppressor gene {anti-oncogene} is mutated
8. Oral cancer is considered to be a multifactorial disease in
which:
Theory of Carcinogenesis:
– The theory of carcinogenesis suggests that cancer develops in
two-stage processes.
– These two stage processes include an initiation stage followed
by a promotion stage:
• It involves being exposed to a specific
carcinogenic agent
Initiation
Stage
• It occurs by either being continuously
exposed to this specific carcinogenic
agent or to non-specific irritants
Promotion
Stage
There is no detection of a single specific cause for oral
cancer
Many factors tend to be likely included in the etiology of
oral cancer as these vary in several groups
9. Etiological factors:
– Several factors are involved in the human cancer:
– Carcinogenesis usually involves combination of these intrinsic &
extrinsic factors >>> complimentary effects
– The main intrinsic & extrinsic factors that may cause oral cancer
are:
carcinogens
(tobacco
smoke, alcohol,
chemicals ...)
abnormalities
in the genetic
material
cancer
direct local
extrinsic effect
• tobacco
• sunlight
• iron deficiency (makes the host more
susceptible to carcinogen's effect)
• alcohol
tobacco alcohol
diet &
nutritional
deficiency
radiation & UV
rays
infectious
agents
dental factors immunosuppresion occupation
precancerous
lesions
10. tobacco
chronic
irritation
damage
of oral
mucosal
cells
1-Tobacco:
– It is the primary & most important risk factor for developing oral
cancer
– 75% of oral cancers are referred to the use of smoked & smokeless
tobacco
– This rate increases with:
Smoking tobacco: (cigarettes, pipe, cigar …)
4000 chemical
agents + > 60
carcinogens (CO,
tar, arsenic, Pb...)
the amount smoked/ chewed
usage duration
cigar
cigarette
pipe
11. Cigar & pipe smokers are at higher risk for having oral cancer
than cigarette smokers
Reverse smoking:
Heat & smoke
from cigar,
cigarettes &
pipe
irritate the
mucous
membranes of
the mouth
• 6x more prone to have oral cancer
cigar smokers (who inhale deeply)
• static contact of the pipe stem with the lower lip
>>> high risk for lip cancer
pipe smokers
holding the lighted end of the
cigarette inside the mouth
common in women
wide spread in indea, South
America & other countries
12. Smokeless tobacco:
Snuff tobacco:
Snuff is a finely ground or powdered tobacco
It may be inhaled:
Dry
Moist (snuff-dipping)
reverse
smoking
high
concentrations
of carcinogens
hitting the
palatal surface
in a focal area
palatal
carcinoma
placing a pinch of snuff between
the gum & the cheek or the upper
lip for a prolonged period
hyperkeratotic lesions of the gingiva & buccal mucosa
increased risk for carcinoma
13. Betel quid (pan):
24 hr a
Pan is usually chewed after meal >> aids in the digestion &
produce slight euphoric effect
It is kept in the mouth for a long time (24 hrs/day)
Note: chewing tobacco + snuff >>> irritation from direct
contact with the mucous membranes
2- Alcohol:
– It is the 2nd
risk factor for developing oral cancer
Consists of betel nut + lime wrapped in
betel leaf
Tobacco & other spices are added
according to custom & individual taste
Leukoplakia (where pan is held in the
mouth)
Malignant transformation (development
of papilliferous & ulcerated masses)
Most of oral
cancer patients
drink and
smoke at the
same time
it is difficult to
have alcohol
alone as a
carcinogenic
factor
Alcohol is
regarded as a
promoter
14. – The effect of alcohol occurs through:
– Histological studies reveal atrophy of oral mucosa
– Notes:
the effect of alcohol & tobacco is multiplicative
The risk depends on:
3- Diet & Nutrition
Iron deficiency:
Iron is important to the normal functioning od epithelial
cells
time
dose
its ability to irritate & dry the mucosa (make it more exposed to
carcinogens in tobacco)
its ability to act as a solvent for carcinogens (specially
tobacco)
contaminants & additives with carcinogenic potential
found in it
acting intrinsically through systemic mechanism ( liver damage or
cirrhosis >>> impaired metabolism & nutritional deficiencies >>>
damage the ability of oral mucosa to maintain its barrier function)
15. Plummer- Vinson syndrome
Vitamin A deficiency:
iron deficiency
atrophic or
immature mucosa
more susceptible
to chemical
carcinogens
impaired cell
mediated
immunity
o Also known as Paterson Kelly syndrome
o It is a severe form of iron-deficiency
o Manifested by:
Painful red tongue
Epithelial atrophy
Dysphagia
o Associated with high frequency of oral
squamous cell carcinoma
vitaminA
maintain intact epithelial
tissues as a physical barrier
to infection
protective role in oral
precancer & cancer
16. antioxidants
• vitamin C
• vitamin E
• Beta-caroten
Vitamin C & vitamin E deficiencies:
Antioxidants protects cell against oxidation damage that can
lead to cancer
Note:
4- Radiation & UV rays
Radiotherapy:
high intake of
antioxidants
decreased risk
of oral cancer
o Beta-carotene is a yellow carotenoid
pigment
o It gives a reddish color to plants (such as
carrots & tomatoes)
o It is usually used as a vitamin supplement
because liver can't convert it into vitamin A
decreases the
immune reactivity
produces
abormalities in
the chromosomal
material
17. Radiotherapy to the head & neck region:
The effect is dose-dependent
Sun (Ultraviolet) rays
UV light is a carcinogenic agent
A person with:
increase the risk for the
later development of new
primary oral malignancy
(carcinoma or sarcoma)
routine
dental
radiograph
small
amount of
radiation
not
associated
with oral
mucosa
chronic
sunlight
exposure
compromis
ed
immunity
increased risk
of developing
cancer of the
lower lip
18. Outdoor workers (farmers, fishermen…) >>> more liable to
develop lip and skin cancer
Confined predominantly to fair skinned people
It is rare in dark skinned people
5- Infectious agents
Viral (HPV-HSV-HIV-EBV)
Oncogenic viruses >> play a major role in variety of cancers
However, no virus has definitively been proven to cause oral
cancer
o Actinic cheilosis:
Diffuse premalignant alteration of the lower lip
dark skin
increased
melanin
pegmintation
protection
against UV
light
viral agents
control the host's ability
to regulate normal
growth & proliferation of
the infected cell
facilitate the
malignant
trasnformation
19. Bacterial (syphilis) tongue lesion (3ry stage):
Tongue carcinomas >>> due to the effect of arsenical
compounds used to treat syphilis
• causes burkitt's lymphoma
Epstein- Barr Virus (EBV)
• increased incidence of Kaposi's sarcoma
HIV
• wide spread in normal epithelium >> it's difficult to cause
oral cancer but they may act with other factors (alcohol,
smoking...)
• HBV 16,18,31,33 subtypes >> detected in oral carcinoma
Human Papilloma Virus (HPV)
• confirmed to cause uterine cervix cancer
• suggested to cause oral caner
Herpes Simplex Virus (HSV)
in the teriary
stage of the
disease
associated
with tongue
carcinoma
(on top of
syphylitic
leukoplakia)
syphilis
20. mechanical
trauma
from
• ill fitting denture
• broken fillings
• sharp edges of teeth
patients having
renal
transplantation
take
immunosuppressive
therapy
newly created
malignant cells
can't be
recognized &
destroyed at an
early stage
increased risk of
oral cancer
Fungal (chronic candidiasis)
Usually associated with speckled leukoplakia (more likely to
undergo malignant transformation)
Fungus >>> suggested to cause this transformation
6- Dental factors
Oral cancer is most common in neglected mouth
Chronic irritation >>> promoter rather than initiator of oral
cancer
7- Immunosuppression
AIDs patients >>> increased risk of oral cancer
the hyphae
interfere
with the cell
metabolism
dysplastic
change
Incriminated in
the etiology of
oral cancer
21. 8- Occupation
References:
1- Ram H, Sarkar J, Kumar H, Konwar R, Bhatt M, Mohammad S. Oral
Cancer: Risk Factors and Molecular Pathogenesis. Journal of
Maxillofacial and Oral Surgery. 2011;10(2):132-137.
2- Kumar M, Nanavati R, Modi T, Dobariya C. Oral cancer: Etiology
and risk factors: A review. Journal of Cancer Research and
Therapeutics. 2016;12(2):458.
increased risk
of having oral
carcinomas
specially those
exposed to raw
cotton & wool
textile workers
increased risk of
having oral
carcinomas
workers in the
printing trades
