ORAL CANCER
SOYEBO O.A.
Den/2005/075
OUTLINE
• INTRODUCTION.
• DEFINITION.
• EPIDEMIOLOGY.
• ORAL CANCER AND PRECANCER
• RISK FACTORS.
• PREVENTION, DIAGNOSIS AND MANAGEMENT
• CONCLUSION
INTRODUCTION
• Oral cancer is one of the ten most
common malignancies in the world
• In developing countries it constitutes
the 3rd commonest malignancy
• Sites: lips and other intra-oral sites
but Para-oral sites such as the
salivary glands, the oropharynx,
nasopharynx and hypopharynx are
not normally included
DEFINITION
• Neoplasm: an abnormal tissue that grows by
cellular proliferation more rapidly than normal
tissue and continues to grow after the stimuli
that initiated the new growth cease.
• Neoplasm show partial or complete lack of
structural organization and functional
coordination with the normal tissue.
• Cancer – general term for malignant neoplasm
EPIDEMIOLOGY
• It is one of the ten most common malignancies
in the world.
• In Asia however, it accounts for over 40% of all
cancers
• Although there is paucity of data on the
epidemiology of the disease in Nigeria, an
increase in the number of oral cancer cases
reporting to general specialist and teaching
hospitals has been observed.
• Over 80% of the malignant neoplasm of the oro-
facial region are squamous cell carcinomas of the
oral mucosa, tongue and lip.
• It usually occurs in people above 40yrs of age
though, in high prevalent areas such as India,
Brazil, New Guinea, France and in Western
Europe, where the teenagers use oral snuff, the
incidence of oral cancer has been recorded in
people below the ages of 35yrs.
• Males are often affected more than females
ORAL CANCER AND PRECANCER
• Oral cancer: lips and other intra-oral sites.
– In the biology of oral cancer, it is now accepted that
series of discrete events take place which eventually
summate to form invasive neoplasm
– During oral carcinogenesis, aetiological factors may
damage cells at the level of DNA
– We can therefore assume that most if not all oral
cancers develop from cells which have survived a
succession of insults at the gene level and that in a
proportion of cases there may be distinguishing at
the clinical and histological level which indicate
precancerous change
• The WHO defined a precancerous lesion as
– “a generalized state associated with a significant
increased risk of cancer”
• Leukoplakia and Erythroplakia constitute the
important precancerous lesions
• Leukoplakia: a white patch or plaque that
cannot be rubbed off and cannot be
characterized clinically or histologically as any
other disease.
– It must in addition not be associated with any
physical or chemical causative agent except the
use of tobacco.
• Erythroplakia: a red patch that cannot be
characterized histologically or clinically as due
to any other condition.
– It is far less common than leukoplakia but it has a
higher malignant potential.
RISK AREAS
• Floor of the mouth
• Lateral border of the tongue
• Lower buccal sulcus
• Alveolus
• Angle of the mouth
PRECANCEROUS LESIONS PRECANCEROUS CONDITIONS
Leukoplakia
Erythroplakia
Syphilis
Sideropenic dysphagia
Submucous fibrosis
Lichen planus
Discoid lupus erythematosus
Actinic keratosis
Sublingual keratosis
RISK FACTORS
• Tobacco
• Alcohol
• Diet and Nutrition
• Ultraviolet light
• Fungal and Viral infection
• Habits
• Chronic Irritation
• Immunodeficiency/ Suppression
• Occupational Risk
TOBACCO
• Major source of intra-oral carcinogen.
• All forms of tobacco consumption have been linked.
– South east Asia: bethel quid
– North Africa and Middle East: a mixture of Tobacco
and lime water or oil called naswar or nash
– It could be held in the mouth
– Smoked in crude cigars or factory made cigarettes
• Carcinogens in tobacco: Nitrosamine (nicotine), the polycyclic
aromatic hydrocarbons (3,4-benzopyrene)
ALCOHOL
• 2nd major risk factor
• Associated with cancer of the floor of the mouth
and tongue.
• Excess consumption of EVERY TYPE of alcohol
(including “hard” liquor, wine, and Beer) raises
the risk status of oral cancer
• Potentiates the effects of tobacco
• Mechanism(s)
• Dehydrating effects of alcohol on the mucosa,
• increasing mucosal permeability,
• Irritation of mucosa
• and it also acts as a solvent for carcinogens
(especially those in tobacco)
DIET AND NUTRITION
• Deficiency of vitamin C, vitamin E , beta
carotene is a precursor of vitamin A and
vitamin A has been linked to oral cancer.
• Adequate consumption of raw vegetables and
fresh fruits gives a lower risk of oral and
pharyngeal cancer.
• Mechanism: Atrophy of oral mucosa
membrane.
• This render them more susceptible to
carcinogens.
ULTRAVIOLET LIGHT
• Causes
– Basal cell carcinoma of the skin
– carcinoma of the vermilion border of the lips
especially in people with outdoor occupation.
• Affects men more.
FUNGAL INFECTION
• Candida albicans has been implicated in oral
squamous cell carcinoma.
• Also found in oral red and white patches with
malignant potentials.
• Mechanisms
– Production of enzymes which produce genotoxic
metabolites
– Its hyphae carrying oncogenes like Ras
VIRAL INFECTION
• Human papilloma virus types 16 and 18
• Epstein Barr virus (naso-pharyngeal
carcinoma)
HABITS
• Chewing of betel quids and areca nuts,
especially when mixed with tobacco increases
the risk of developing oral cancer.
• Areca has been associated with the
development of Submucous fibrosis
• Use of clay pipe has been associated with lip
cancer (thermal irritation)
CHRONIC IRRITATION
• It is possible that chronic trauma, in addition
to other carcinogens, may promote the
transformation of epithelial cells.
• Dental calculus, ill fitting dentures, jagged
edges of restorations may play a role in
localizing the site of tumor development.
IMMUNE DEFICIENCY/
SUPPRESSION
• It could b drug induced or as a result of HIV
infection which could render patients
susceptible to oncogenic viruses
• However a definite relationship between
immune suppression and oral cancer is yet to
be established.
OCCUPATIONAL RISK
• Plays a minor role
• Exposure to the following have been associated
with oropharyngeal and laryngeal cancer;
– Cement
– Coal products
– Wood dust
– Organic chemicals
– Nickel dust
• Occupational exposure to Ultraviolet rays from
sunlight has been associated with cancer of the
lips
DIAGNOSIS
• Diagnosis of oral cancer and precancer depends
on the medical and dental history and clinical
examination supplemented by investigations
• Any chronic oral lesion should be regarded with
suspicion especially in an older patient or
associated with any of the precancerous lesions
and conditions outlined below
• Extra caution must also be taken if lesion is
indurated, fixed, attached to the underlying
tissue, associated with lymphadenopathy.
Prognostic factors
• Tumor size: <2cm
• Depth of infiltration: <5mm
• Site : lips > oral cavity > oropharynx
• Lymph nodes: presence of clinically positive or
fixed lymph nodes gives worse prognosis
PREVENTION.
• Prevention involves interventions aimed at
eliminating, eradicating or minimizing the
impact of the disease
• PRIMORDIAL
• Avoid the emergence and establishment of the
patterns of living that are known to contribute to
an elevated risk of disease
• PRIMARY: Reduce the incidence of cancer and
precancer.It is aimed reducing the number of new cases.
– Discourage smoking and alcohol consumption
– Encourage good oral hygiene
– Encourage balanced diet
– Use of hat in sunlight for farmers
– Wearing of facemasks for factory workers
involved with chemicals and metals
– Health education
PREVENTION.
• SECONDARY: aimed at detection of cancer at
an early stage
• Early detection, especially at the
precancerous stage, offers a better prognosis
with a better chance of cure.
› Public education on early signs and self
examination
› Screening
PREVENTION.
• TERTIARY: Treat late stage of disease and
complications
MANAGEMENT
• Pre-malignant lesions (precancer)
– Management of pre-malignant lesions is guided
for the most part, by the degree of dysplasia
present irrespective of clinical appearance.
– Dysplasia (mild, moderate, severe)
– Non-intervention and intervention strategies may
be adopted depending on the degree of dysplasia.
Non-intervention strategies
• Patients with histologic ally proven mild or
moderate dysplastic lesion may be placed on
“non-intervention follow-up” in which case
the patient is reviewed regularly every 3-
6months and carefully examined for any
changes in the lesion which would necessitate
any further biopsy
• If the lesion appears clinically unchanged, it
should still be necessary to perform a repeat
biopsy no longer than 3yrs after the initial
biopsy
• Throughout the period of review, repeat
attempts at candida isolation and
venopuncture should be undertaken to ensure
that infection or nutritional deficiency has not
developed and advice should be given in
relation to smoking and alcohol.
Intervention Strategies
• The main method of active therapy for pre-
malignant lesions are:
– Surgical excision
– Topical cytotoxic therapy
– Cryosurgery and laser therapy
• Management often depends largely on the
experience of clinician as well as the facilities
available at the treatment centre
MALIGNANT LESIONS (oral caner)
• For many years, surgery and/or radiotherapy
has been used as a curative modality
• The aim of treatment depends on the stage of
presentation
– Early lesions: can completely be treated by surgery
or radiotherapy.
– Late lesions: a palliative treatment is advocated.
This could be in the form of radiotherapy, surgery
or both.
• Rehabilitation of patient after surgery could
be either surgical reconstruction, prosthetic
reconstruction or both.
• This is aimed at restoring esthetics, function
and speech.
• All patients must be placed on life-long review
of about 6monthly intervals during which risk
factors should be continually assessed.
CONCLUSION
• In developing countries, including Nigeria,
where resources are severely limited,
preventive measures should take priority in
the management and control of oral cancer.
• Detailed oral examination directed at
identifying precancerous lesions must always
be part of routine medical and dental
examinations particularly in patients above
the age of 35yrs
• It is also necessary that all dental and medical
practitioners should be familiar with the signs
and symptoms of oral precancer and cancer
because this would enhance early diagnosis
which is very crucial in the management of
this disease.

Oral cancer

  • 1.
  • 2.
    OUTLINE • INTRODUCTION. • DEFINITION. •EPIDEMIOLOGY. • ORAL CANCER AND PRECANCER • RISK FACTORS. • PREVENTION, DIAGNOSIS AND MANAGEMENT • CONCLUSION
  • 3.
    INTRODUCTION • Oral canceris one of the ten most common malignancies in the world • In developing countries it constitutes the 3rd commonest malignancy • Sites: lips and other intra-oral sites but Para-oral sites such as the salivary glands, the oropharynx, nasopharynx and hypopharynx are not normally included
  • 4.
    DEFINITION • Neoplasm: anabnormal tissue that grows by cellular proliferation more rapidly than normal tissue and continues to grow after the stimuli that initiated the new growth cease. • Neoplasm show partial or complete lack of structural organization and functional coordination with the normal tissue. • Cancer – general term for malignant neoplasm
  • 5.
    EPIDEMIOLOGY • It isone of the ten most common malignancies in the world. • In Asia however, it accounts for over 40% of all cancers • Although there is paucity of data on the epidemiology of the disease in Nigeria, an increase in the number of oral cancer cases reporting to general specialist and teaching hospitals has been observed.
  • 6.
    • Over 80%of the malignant neoplasm of the oro- facial region are squamous cell carcinomas of the oral mucosa, tongue and lip. • It usually occurs in people above 40yrs of age though, in high prevalent areas such as India, Brazil, New Guinea, France and in Western Europe, where the teenagers use oral snuff, the incidence of oral cancer has been recorded in people below the ages of 35yrs. • Males are often affected more than females
  • 7.
    ORAL CANCER ANDPRECANCER • Oral cancer: lips and other intra-oral sites. – In the biology of oral cancer, it is now accepted that series of discrete events take place which eventually summate to form invasive neoplasm – During oral carcinogenesis, aetiological factors may damage cells at the level of DNA – We can therefore assume that most if not all oral cancers develop from cells which have survived a succession of insults at the gene level and that in a proportion of cases there may be distinguishing at the clinical and histological level which indicate precancerous change
  • 8.
    • The WHOdefined a precancerous lesion as – “a generalized state associated with a significant increased risk of cancer” • Leukoplakia and Erythroplakia constitute the important precancerous lesions
  • 9.
    • Leukoplakia: awhite patch or plaque that cannot be rubbed off and cannot be characterized clinically or histologically as any other disease. – It must in addition not be associated with any physical or chemical causative agent except the use of tobacco. • Erythroplakia: a red patch that cannot be characterized histologically or clinically as due to any other condition. – It is far less common than leukoplakia but it has a higher malignant potential.
  • 10.
    RISK AREAS • Floorof the mouth • Lateral border of the tongue • Lower buccal sulcus • Alveolus • Angle of the mouth
  • 12.
    PRECANCEROUS LESIONS PRECANCEROUSCONDITIONS Leukoplakia Erythroplakia Syphilis Sideropenic dysphagia Submucous fibrosis Lichen planus Discoid lupus erythematosus Actinic keratosis Sublingual keratosis
  • 13.
    RISK FACTORS • Tobacco •Alcohol • Diet and Nutrition • Ultraviolet light • Fungal and Viral infection • Habits • Chronic Irritation • Immunodeficiency/ Suppression • Occupational Risk
  • 14.
    TOBACCO • Major sourceof intra-oral carcinogen. • All forms of tobacco consumption have been linked. – South east Asia: bethel quid – North Africa and Middle East: a mixture of Tobacco and lime water or oil called naswar or nash – It could be held in the mouth – Smoked in crude cigars or factory made cigarettes • Carcinogens in tobacco: Nitrosamine (nicotine), the polycyclic aromatic hydrocarbons (3,4-benzopyrene)
  • 15.
    ALCOHOL • 2nd majorrisk factor • Associated with cancer of the floor of the mouth and tongue. • Excess consumption of EVERY TYPE of alcohol (including “hard” liquor, wine, and Beer) raises the risk status of oral cancer • Potentiates the effects of tobacco • Mechanism(s) • Dehydrating effects of alcohol on the mucosa, • increasing mucosal permeability, • Irritation of mucosa • and it also acts as a solvent for carcinogens (especially those in tobacco)
  • 16.
    DIET AND NUTRITION •Deficiency of vitamin C, vitamin E , beta carotene is a precursor of vitamin A and vitamin A has been linked to oral cancer. • Adequate consumption of raw vegetables and fresh fruits gives a lower risk of oral and pharyngeal cancer. • Mechanism: Atrophy of oral mucosa membrane. • This render them more susceptible to carcinogens.
  • 17.
    ULTRAVIOLET LIGHT • Causes –Basal cell carcinoma of the skin – carcinoma of the vermilion border of the lips especially in people with outdoor occupation. • Affects men more.
  • 18.
    FUNGAL INFECTION • Candidaalbicans has been implicated in oral squamous cell carcinoma. • Also found in oral red and white patches with malignant potentials. • Mechanisms – Production of enzymes which produce genotoxic metabolites – Its hyphae carrying oncogenes like Ras
  • 19.
    VIRAL INFECTION • Humanpapilloma virus types 16 and 18 • Epstein Barr virus (naso-pharyngeal carcinoma)
  • 20.
    HABITS • Chewing ofbetel quids and areca nuts, especially when mixed with tobacco increases the risk of developing oral cancer. • Areca has been associated with the development of Submucous fibrosis • Use of clay pipe has been associated with lip cancer (thermal irritation)
  • 21.
    CHRONIC IRRITATION • Itis possible that chronic trauma, in addition to other carcinogens, may promote the transformation of epithelial cells. • Dental calculus, ill fitting dentures, jagged edges of restorations may play a role in localizing the site of tumor development.
  • 22.
    IMMUNE DEFICIENCY/ SUPPRESSION • Itcould b drug induced or as a result of HIV infection which could render patients susceptible to oncogenic viruses • However a definite relationship between immune suppression and oral cancer is yet to be established.
  • 23.
    OCCUPATIONAL RISK • Playsa minor role • Exposure to the following have been associated with oropharyngeal and laryngeal cancer; – Cement – Coal products – Wood dust – Organic chemicals – Nickel dust • Occupational exposure to Ultraviolet rays from sunlight has been associated with cancer of the lips
  • 24.
    DIAGNOSIS • Diagnosis oforal cancer and precancer depends on the medical and dental history and clinical examination supplemented by investigations • Any chronic oral lesion should be regarded with suspicion especially in an older patient or associated with any of the precancerous lesions and conditions outlined below • Extra caution must also be taken if lesion is indurated, fixed, attached to the underlying tissue, associated with lymphadenopathy.
  • 25.
    Prognostic factors • Tumorsize: <2cm • Depth of infiltration: <5mm • Site : lips > oral cavity > oropharynx • Lymph nodes: presence of clinically positive or fixed lymph nodes gives worse prognosis
  • 26.
    PREVENTION. • Prevention involvesinterventions aimed at eliminating, eradicating or minimizing the impact of the disease • PRIMORDIAL • Avoid the emergence and establishment of the patterns of living that are known to contribute to an elevated risk of disease
  • 27.
    • PRIMARY: Reducethe incidence of cancer and precancer.It is aimed reducing the number of new cases. – Discourage smoking and alcohol consumption – Encourage good oral hygiene – Encourage balanced diet – Use of hat in sunlight for farmers – Wearing of facemasks for factory workers involved with chemicals and metals – Health education
  • 28.
    PREVENTION. • SECONDARY: aimedat detection of cancer at an early stage • Early detection, especially at the precancerous stage, offers a better prognosis with a better chance of cure. › Public education on early signs and self examination › Screening
  • 29.
    PREVENTION. • TERTIARY: Treatlate stage of disease and complications
  • 30.
    MANAGEMENT • Pre-malignant lesions(precancer) – Management of pre-malignant lesions is guided for the most part, by the degree of dysplasia present irrespective of clinical appearance. – Dysplasia (mild, moderate, severe) – Non-intervention and intervention strategies may be adopted depending on the degree of dysplasia.
  • 31.
    Non-intervention strategies • Patientswith histologic ally proven mild or moderate dysplastic lesion may be placed on “non-intervention follow-up” in which case the patient is reviewed regularly every 3- 6months and carefully examined for any changes in the lesion which would necessitate any further biopsy • If the lesion appears clinically unchanged, it should still be necessary to perform a repeat biopsy no longer than 3yrs after the initial biopsy
  • 32.
    • Throughout theperiod of review, repeat attempts at candida isolation and venopuncture should be undertaken to ensure that infection or nutritional deficiency has not developed and advice should be given in relation to smoking and alcohol.
  • 33.
    Intervention Strategies • Themain method of active therapy for pre- malignant lesions are: – Surgical excision – Topical cytotoxic therapy – Cryosurgery and laser therapy • Management often depends largely on the experience of clinician as well as the facilities available at the treatment centre
  • 34.
    MALIGNANT LESIONS (oralcaner) • For many years, surgery and/or radiotherapy has been used as a curative modality • The aim of treatment depends on the stage of presentation – Early lesions: can completely be treated by surgery or radiotherapy. – Late lesions: a palliative treatment is advocated. This could be in the form of radiotherapy, surgery or both.
  • 35.
    • Rehabilitation ofpatient after surgery could be either surgical reconstruction, prosthetic reconstruction or both. • This is aimed at restoring esthetics, function and speech. • All patients must be placed on life-long review of about 6monthly intervals during which risk factors should be continually assessed.
  • 36.
    CONCLUSION • In developingcountries, including Nigeria, where resources are severely limited, preventive measures should take priority in the management and control of oral cancer. • Detailed oral examination directed at identifying precancerous lesions must always be part of routine medical and dental examinations particularly in patients above the age of 35yrs
  • 37.
    • It isalso necessary that all dental and medical practitioners should be familiar with the signs and symptoms of oral precancer and cancer because this would enhance early diagnosis which is very crucial in the management of this disease.