Download Oral Cancer

Prevention of oral squamous
carcinoma
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Indidence, survival
• About 36,000 American patient will be
diagnosed with oral or pharyngeal cancer this
year
• It will cause over 8,000 deaths, killing roughly
1 person per hour
• Of the newly diagnosed individuals, only half
will be alive in 5 years
• This is a number which has not significantly
improved in decades
Mortality of oral cancer in Hungary
(1948-99)
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Mortality of OSCC in Mid-Eastern Europe
(1992-1995)
Besides the metastasis,
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Mortality
• The death rate for oral cancer is higher than that of
cervical cancer, Hodgkins disease, cancer of the
brain, liver, testes, kidney, or skin cancer (malignant
melanoma
• Together with cancer of the larynx, for which the risk
factors are the same, the numbers of diagnosed
cases are over 350,000 to 400,000 new cases being
found each year worldwide
Mortality of OSCC
• The death rate associated with this OSCC is especially
high because this disease is routinely discovered late
in its development
• Often it is discovered when the cancer has
metastasized to another location, especially to the
lymph nodes of the neck
• Prognosis at this stage of discovery is significantly
worse than when it is diagnosed localized in the oral
cavity
• at these later stages, the primary tumor has had time
to invade deep into local structures besides the
metastasis
oral cancer
• Oral squamous cell cancer persist and grew on the head and neck
above the level of the clavicle untill the most advanced phases of the
disease
• Left untreated, oral cancers allways lead to death of the patient
within 1,5-2 years, due to local invasion to the surrounding tissues,
and metastases on the neck, rarely to the bones and lungs)
• The most common causes of death are marasmus, erosion bleeding
from the great vessels (e.g. int. or external carotid artery,)
• Inability of eating, drinking due to pharyngeal masses necessitates
arteficial nutrition via surgical or percutaneous gastrostomy,
• Tumorous upper airway obstruction necessitates tracheostomy
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Factors determining survival
• Oral cancer is particularly dangerous because it
has a high risk of producing second primary
tumors ( at a different site of oral cavity)
• Patients who survive a first encounter with the
disease, have up to a 20 times higher risk of
developing a second cancer!
• This heightened risk factor can last for 5 to 10
years after the first occurrence
• There are several types of oral cancers, but 90%
are squamous cell carcinomas
Factors of etiology
Smoking
Drinking Alcohol
Poor oral hygiene
Viruses
Poor fitting prosthesis
Etiology
• The human papilloma virus, particularly
versions 16 and 18, a sexually transmitted
infection between partners,
• possible association with the increasing
incidence of young non-smoking oral cancer
patients
• This virus is the causative agent in more than
90% of all cervical (gynecological) cancers
Demographics
• For decades OSCC has been a cancer which
affected 6 men for every woman
• That ratio has now become 2 men to each woman
Demographics
• Age is a risk factor for oral cancer, as most of
the time it occurs in those over the age of 40
• The age of diagnosed patients may indicate a
time component in the biochemical or
biophysical processes of aging cells that allows
malignant transformation, or perhaps,
immune system competence diminishes with
age
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Risk factors
• the accumulative damage from other factors, such as
tobacco use, and alcohol consumption are
responsible
• Alcohol and smoking have a synergistic effect in the
carcinogenesis in the oral cavity
• It may take several decades of smoking to precipitate
the development of a cancer
• ( cca. 95% of oral cancer patients have been smoking
for 3-4 decades )
Risk factors
• Tobacco- 75% of all dx tobacco users
• Alcohol- heavy usage
• Alcohol + Tobacco- Those who both smoke and drink,
have a 15 times greater risk of developing oral cancer
than others
– Considered both chemical and lifestyle factors
• Ultraviolet radiation- lip and skin cancers
– Have decreased over the years due to use of sunblocks and
education
• Radiation exposure ( enviromental and industrial
/due to profession/ )
Risk factors
• Biologic Factors
– Viral and fungal infection
– HPV is a common, sexually transmitted virus, e.g
about 40 million individuals are infected in USA
• 1% of those infected, have the HPV16 strain
which is a causative agent in cervical cancer,
and now is linked to oral cancer as well
Risk factors
• Risk factors exert their carcinogenic effects on
the entire oral cavity, paryngeal , upper aerodigestive system mucosa ( so called fieldcancerization !)
• Bronchial, laryngeal, esophageal cancer !!!
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Signs and symptoms
• In its early stages, it can go unnoticed
• It can be painless, and little in the way of
physical changes may be obvious
• dentists or doctors can see or feel the
precursor tissue changes, or the actual cancer
while it is still very small, or in its earliest
stages
symptoms
• White or red patch in the oral cavity
• Small indurated ulcer
• Many benign tissue changes that occur normally in
your mouth, and some things as simple as a bite on
the inside of your cheek may mimic the look of a
dangerous tissue change.
• It is important : any sore or discolored areain the oral
cavity , which does not heal within 14 days, should
be looked at by an oral and maxillofacial surgeon !!
Signs and symptoms
• Lump or mass in the mouth or felt in neck
• Pain or difficulty in swallowing, speaking or
chewing
• Wart like lesion
• Common areas
– Lip
– Tongue
– Floor of mouth
Progression of OSCC
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Hyperkeratosis
Dysplasia
Erythroplakia
Carcinoma in situ
Invasive carcinoma
Hyperkeratosis
• Excessively thickened layer of the stratum corneum
composed of orthokeratin (hyperorthokeratosis) or
parakeratin (hyperparakeratosis).
• Clinical features:
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mucosal lesion anywhere in the oral cavity
appears lighter in color than the normal color
flat or raised
may be rough
duration may be weeks to months
cannot be wiped off
usually adult occurance
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Hyperkeratosis
• Etiology
– chronic irritant
• Thickened keratin layer
• Organized connective tissue layer
• Possible to have inflammatory reaction in
connective tissue due to irritation
• Normal maturation of epithelial cells
• No evidence of dysplasia
Hyperkeratosis
• Main Pathologic Process
– benign hyperkeratosis
• Treatment
– removing cause of lesion
– may be excised
• Prognosis
– good
Dysplasia
• A pre-malignant change in epithelium
characterized by a combination of
individual cell and architectural alterations
• Clinical features
– white leukoplakic lesion of the oral mucosa
– duration varies from months to years
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Differential diagnosis:
hyperkeratosis
squamous cell carcinoma
epthelial dysplasia
lichen planus
Displasia
Histology
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basal cell proliferation
pleomorphism (cell variation)
mitotic activity,
hyperchromatic nuclei
dyskeratosis (abnormal keratosis)
premalignant (cellular change in the
epithelium and noinvasion into the
connective tissue)
Dysplasia - treatment
• Removal of the cause
• biopsy the lesion to determine severity of
dysplasia
• PROGNOSIS:
• may regress to normal in early stages
• usually considered to be premalignant
Erythroplakia
• Chronic red oral mucosal patch usually not
attributed to traumatic, vascular or
inflammatory causes but frequently caused by
epithelial dysplasia, ca in situ, or squamous
cell carcinoma.
• asymptomatic red macule or patch on a on a
mucosal surface
• floor of mouth, tongue and palate
• multiple lesions may be present
Erythroplakia
• typical oral lesion is less than 1.5 cm.
• well-demarcated from the surrounding pink mucosa
• surface is typically a smooth, soft, velvety texture and
regular in coloration
• predominantly a disease of older males
• a lack of keratin production in the epithelium
• thin atrophic epithelium covering the underlying
microvasculature
• underlying connective tissue often demonstrates chronic
inflammation along with increase in size and number of
vascular structures
Differential diagnosis
• atrophic candidiasis
• erythroplakia
• focal inflammed mucosa
Erythroplakia
• Treatment:
• biopsy to determine the exact nature of
the lesion
• Prognosis
– depends on the specific histopathologic
diagnosis
Carcinoma in Situ
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White, red, or red/white patch on lining mucosa; may also
appear as a small (<1.0 cm) soft ulcer.
Carcinoma In Situ- Histology
• Anaplasia with or without hyperkeratosis; no
invasion
• Anaplasia= cells lack differentiation
Oral squamous cell cancer
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Malignant neoplasm of stratified squamous epithelium that is capable of locally
destructive growth and distant metastasis
• possible sites
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lower lip
tongue
floor of the mouth
soft palate
gingival / alveolar ridge
buccal mucosa
more common in adult males
early presentation of leukoplakias and erythroplakias
painless ulcer, tumorous mass, or verrucous (papillary growth)
painless ulcer, tumorous mass, or verrucous (papillary growth)
occasionally loosening or loss of teeth
possible paresthesia of the teeth and lower lip
Differential diagnosis
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squamous cell carcinoma
primary syphilis
tuberculosis
deep fungal infection
traumatic ulcerated granuloma
Histological features
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increased mitotic activity
well differentiated
keratin pearls (abnormal keratinization)
hyperchromatic nuclei
pleomorphism
epithelium islands
connective tissue stroma with chronic inflammation
(histiocytes, lymphocytes, etc.)
OSCC
• Treatment: surgical excision, radiation
therapy or both
• Prognosis: left untreated, metastasis via the
lymphatic vessels most often to the lungs and
liver
complex oncological treatment
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Reduce risk factors
Regular Screening
Early detection
Appropriate treatment ( surgical, radiotherapy,
chemotherapy, psychological,surgical and dental
rehabilitation)
Prevention
• Thorough examination of the oral cavity
and head and neck region is essential part
of all dental and medical examination!
• Alcohol consumption and smoking should
be cleared among anamnestic data
• Meticulous inspection and palpation of the
oral cavity, face and the neck requires:
» Proper lighting
» Dental mouth mirror
» Gauze squares
» Gloves
» 5 minutes
Prevention
• Avoiding risk factors and increasing protective factors may help
prevent cancer.
• The following risk factors may increase the risk of oral cancer:
– Tobacco use
– Alcohol use
– Sun exposure
– HPV infection
• Majority of OSCC cases can be prevented by avoiding the risk factors
• Quitting smoking (reduces the risk of oral cancer by one-half (50%)
within 5 years. Within 10 years of quitting, the risk of oral cancer is the
same as for a person who never used tobacco)
Prevention
• The protective factors may decrease the risk of oral cancer:
• Dietary factors
– Chemoprevention
• Cancer prevention clinical trials are used to study ways to
prevent cancer.
• New ways to prevent oral cancer are being studied in
clinical trials.
• Education of self-examination of the risk patients
• Regular check-ups for risk patients
Chemoprevention
Use of drugs, vitamins or other agents to prevent or delay the growth of cancer
The purpose of some cancer prevention clinical trials is to find out
whether actions people take can prevent cancer.
These may include eating fruits and vegetables, exercising, quitting smoking,
or taking certain medicines, vitamins, minerals, or food supplements
Erlotinib Prevention of Oral Cancer (EPOC)
Secondary Primary Tumor Prevention With EGFR, OSI-774, and Cyclooxygenase-2
Phase I/II Study of Chemoprevention With EGFR and COX-2 Inhibitor
Clinical Evaluation of Bioadhesive Gels for Oral Cancer Chemoprevention
Lyophilized Black Raspberries in Preventing Oral Cancer in High-Risk Patients
Previously Diagnosed With Stage I-IV or In Situ Head and Neck Cancer
Bowman-Birk Inhibitor Concentrate in Preventing Cancer in Patients With Oral
Leukoplakia
Vandetanib in Preventing Head and Neck Cancer in Patients With Precancerous
Head and Neck Lesions
Phase I Chemoprevention Trial With Green Tea Polyphenon E and Erlotinib in
Patients With Premalignant Lesions of the Head and Neck
A Randomized Study of Sulindac in Oral Premalignant Lesions