Oral CA Lec (Compatibility Mode)

Oral Cancer
Maria Fornatora, D.M.D., Diplomate ABOP

Director, Division of Oral and Maxillofacial Pathology
Temple University, Kornberg School of Dentistry
Oral Cancer Quiz
 True/False. Oral cancer ________.
 is more common than cervical cancer and melanoma
combined.
 has an overall death rate of 50% which has not
change in 50 years.
 has a multifactorial cause.
 is most often diagnosed in the late stages.
 is readily visible to the unaided eye even in early and

precancer stages.
U.S. Oral CANCER
STATISTICS
 Cancer of the H&N is the 5th most common
cancer in the world
 “H&N: oral cavity, throat and larynx”
 “Oral: oral cavity and oropharynx”
 31,OOO NEW CASES Oral Cancer in US

YEARLY
 More common than cervical cancer and melanoma combined
 Causes more deaths/yr than cervical cancer or
skin cancer
U.S. OROPHARYNGEAL
CANCER STATISTICS
 Overall 5 year survival rate 50%

 50% of patients have distant spread at time of diagnosis
 Mortality rate has remained unchanged for last 50 years
 8,000 Americans die of OC/yr (1 per hour)
 Early detection=improved survival

Oral CANCER
 Over 95% Oral Cancer is the squamous cell
carcinoma type (SCCa)
 SCCa arises from the surface mucosal epithelium

of the mouth and throat
Oral CANCER
 Tongue=50% of Oral Ca in US (esp
post lateral and ventral)
 Floorof the mouth =35% of Oral Ca in

US (more common in men), very
associated with the development of
second primary of aerodigestive tract
Oral SQUAMOUS CELL CARCINOMA
Gender and Age
Gender and Age
 Male : female ratio 1.8:1
 Develops predominantly between

 ages 50 – 70 years in men and
 60 – 80 years in women
 Between 1 – 3% of case develop under age 40

 Young patients do not have the usual risk factors
Oral SQUAMOUS CELL CARCINOMA
US Incidence Trends: Gender
 Prior to 1940 male : female ratio - 10:1

 1980s ratio 3:1
 Current ratio 1.8:1
 Reason: The major risk factor for OPH Ca is

smoking. And tobacco use among women has
steadily increased in women beginning in the
early decades of the century
Etiology of Oral Cancer
 DNA damage
 Mucosal stem cells (in the basal layer) self renew
and also generate daughter cells that divide more
rapidly (parabasal layers) and undergo maturity to
terminal differentiation
 Mucosal stem cells and their daughter cells
undergo continuous assault from carcinogens
(e.g.tobacco) and oncogenic viruses (e.g. HPV)
which cause DNA damage (also spontaneous)
 Damaged DNA in mucosal stem cells may be

repaired by the cell (your previous lecture) or
may remain to be maintained in the self renewal
process and transmitted to daughter cells
 Genetically damaged daughter cells and stem cells
are continuously exposed to new carcinogens (e.g
cigarette smoke) and co-carcinogens (e.g. alcohol)
& can eventually be transformed into a malignant
cell undergoing uncontrolled division (Multiple hit
theory of carcinogenesis)
 Critical #/event? Est. 5 events in humans are
required to transform a normal cell to a cancer cell
Boudewijn, et al J oral Path Med, 2003
 The genetic alterations: tumor suppressor gene

inactivated by mutation (eg p53) or oncogene
activated by mutation or amplification
RISK FACTORS/Carcinogens
Tobacco (esp. smoking)

Alcohol
Actinic radiation
Human papillomavirus infection (HPV)
Iron deficiency
Tobacco smoking
 Most popular in US in the 1940s
 Declining prevalence (65% in 1940s; 25% today

in US)
Smoking and Cancer
Lung cancer emerges as a threat to the
tobacco industry in 1940s
 1946: R.J. Reynolds’
Campaign For the
Camels Brand
Post-war cigarette
advertising: lung cancer
emerges as a threat to the
tobacco industry. To
reassure a worried public
was to incorporate
images of physicians in
their ads
Tobacco smoking
 1950-1960 definitive evidence (epidemiologic

and laboratory studies) linking smoking to lung
cancer
 Mostly indirect clinical evidence that implicates

tobacco smoking in the development of oral
SCCa
 80% of oral cancer pts smoke
TOBACCO & ALCOHOL
 Effects are synergistic
 Some studies show people who smoke and drink

have 15X increased risk
ALCOHOL
 Risk of dysplasia (precancer) 2X greater than in

nondrinkers
 Risk is however dose and time dependent

Radiation
 UV radiation and x-irradiation from
radiotherapy to the head and neck causes
decrease in immune reactivity and DNA damage
 Dose dependent risk

Role of Viruses
 Epstein Barr virus -
Burkitt’s lymphoma, nasopharyngeal ca in
China
 Human papillomavirus,
high risk - HPV 16,18,31,32
low risk - HPV 6, 11
 Herpes Simplex Virus – no evidence
HUMAN PAPILLOMAVIRUS
50% OF HEAD AND NECK CANCERS
ARE INFECTED WITH HUMAN
PAPILLOMAVIRUS
There is increasing evidence that HPV is

responsible for a subset of oral cancers,
especially those of the oropharynx and tonsils
Iron deficiency
 Chronic severe iron deficiency is associate with

impaired cell-mediated immunity and high turn
over rates of upper GI epithelium
Genetic Susceptibility
 Heredity does not appear to play a major
etiologic role in oral cancer
 DNA repair deficiency syndromes

 Bloom syndrome
 Fanconi anemia
 Ataxia-telangiectasia
 Xeroderma pigmentosa –from previous lecture:

Individuals with Xeroderma Pigmentosum are unable to perform
the first step of nucleotide excision repair.
Clinical features of Oral SCCa
and precancer
 Symptoms:
Precancers and early cancers: painless,
asymptomatic
Advanced cancers: pain, paresthesia, lossof
function, mass (at site and/or neck)
 Signs:
 Precancers and cancers cause visible color and
texture changes of the oral mucosa
What does Oral SCCa and
precancer look like clinically?
Leukoplakia (white patch)

Erythroplakia (red patch)
Leukoplakia-erythroplakia (red & white patch)
Chronic Ulcer
ENDOPHYTIC - ULCERATED, DEPRESSED ROLLED BORDER -
INFILTRATION UNDER MUCOSA
Tumorous mass
EXOPHYTIC - IRREGULAR SURFACE USUALLY INDURATED
precancer
precancer
precancer
cancer
cancer
cancer
precancer
cancer
cancer
Oral Cancer Quiz
 True/False. Oral cancer ________.
 is more common than cervical cancer and melanoma
combined.
 has an overall death rate of 50% which has not
change in 50 years.
 has a multifactorial cause.
 is most often diagnosed in the late stages.
 is readily visible to the unaided eye even in early and

precancer stages.
Oral Cancer Screening:
•Visual examination of the oral cavity in
asymptomatic people increases survival
(Kerala Study: inc. survival for males with
high risk habits like tobacco use
•(Lancet 2005;365(9475):1927-33)
•Opportunistic Screening
AAOMP Position paper on Adjunctive Oral
Cancer Diagnostics
Critical evaluation of diagnostic aids for the detection of
oral cancer. Lingen M, Kalmar JR, Karrison T, Speight
PM Oral Oncology 2008 January; 44(1): 10-22.
 Conclusion: Scalpel biopsy is the gold standard for diagnosis.
Noninvasive screening techniques and adjunctive diagnostic
tests such as toluidine blue, brush cytology, tissue reflectance
and autofluorescence should not be considered as substitutes
for biopsy. Moreover, the use of these tests to improve
detection of oral cancers and precancers beyond conventional
oral examination alone has yet to be rigorously confirmed.
Oral Cancer Screening
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Oral Cancer

Maria Fornatora, D.M.D., Diplomate ABOP

 is most often diagnosed in the late stages.

 is readily visible to the unaided eye even in early and

 31,OOO NEW CASES Oral Cancer in US

 Overall 5 year survival rate 50%

 Early detection=improved survival

 SCCa arises from the surface mucosal epithelium

 Floorof the mouth =35% of Oral Ca in

Gender and Age

 Male : female ratio 1.8:1

 Develops predominantly between

 Between 1 – 3% of case develop under age 40

 Prior to 1940 male : female ratio - 10:1

 Reason: The major risk factor for OPH Ca is

 Damaged DNA in mucosal stem cells may be

 The genetic alterations: tumor suppressor gene

Tobacco (esp. smoking)

 Most popular in US in the 1940s

 Declining prevalence (65% in 1940s; 25% today

 1950-1960 definitive evidence (epidemiologic

 Mostly indirect clinical evidence that implicates

 Effects are synergistic

 Some studies show people who smoke and drink

 Risk of dysplasia (precancer) 2X greater than in

 Risk is however dose and time dependent

 Dose dependent risk

There is increasing evidence that HPV is

 Chronic severe iron deficiency is associate with

 DNA repair deficiency syndromes

 Xeroderma pigmentosa –from previous lecture:

Leukoplakia (white patch)

 is most often diagnosed in the late stages.

 is readily visible to the unaided eye even in early and

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