OUTLINE• INTRODUCTION.• DEFINITION.• EPIDEMIOLOGY.• ORAL CANCER AND PRECANCER• RISK FACTORS.• PREVENTION, DIAGNOSIS AND MANAGEMENT• CONCLUSION
INTRODUCTION• Oral cancer is one of the ten mostcommon malignancies in the world• In developing countries it constitutesthe 3rd commonest malignancy• Sites: lips and other intra-oral sitesbut Para-oral sites such as thesalivary glands, the oropharynx,nasopharynx and hypopharynx arenot normally included
DEFINITION• Neoplasm: an abnormal tissue that grows bycellular proliferation more rapidly than normaltissue and continues to grow after the stimulithat initiated the new growth cease.• Neoplasm show partial or complete lack ofstructural organization and functionalcoordination with the normal tissue.• Cancer – general term for malignant neoplasm
EPIDEMIOLOGY• It is one of the ten most common malignanciesin the world.• In Asia however, it accounts for over 40% of allcancers• Although there is paucity of data on theepidemiology of the disease in Nigeria, anincrease in the number of oral cancer casesreporting to general specialist and teachinghospitals has been observed.
• Over 80% of the malignant neoplasm of the oro-facial region are squamous cell carcinomas of theoral mucosa, tongue and lip.• It usually occurs in people above 40yrs of agethough, in high prevalent areas such as India,Brazil, New Guinea, France and in WesternEurope, where the teenagers use oral snuff, theincidence of oral cancer has been recorded inpeople 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 thatseries of discrete events take place which eventuallysummate to form invasive neoplasm– During oral carcinogenesis, aetiological factors maydamage cells at the level of DNA– We can therefore assume that most if not all oralcancers develop from cells which have survived asuccession of insults at the gene level and that in aproportion of cases there may be distinguishing atthe clinical and histological level which indicateprecancerous change
• The WHO defined a precancerous lesion as– “a generalized state associated with a significantincreased risk of cancer”• Leukoplakia and Erythroplakia constitute theimportant precancerous lesions
• Leukoplakia: a white patch or plaque thatcannot be rubbed off and cannot becharacterized clinically or histologically as anyother disease.– It must in addition not be associated with anyphysical or chemical causative agent except theuse of tobacco.• Erythroplakia: a red patch that cannot becharacterized histologically or clinically as dueto any other condition.– It is far less common than leukoplakia but it has ahigher malignant potential.
RISK AREAS• Floor of the mouth• Lateral border of the tongue• Lower buccal sulcus• Alveolus• Angle of the mouth
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 Tobaccoand 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 polycyclicaromatic hydrocarbons (3,4-benzopyrene)
ALCOHOL• 2nd major risk factor• Associated with cancer of the floor of the mouthand tongue.• Excess consumption of EVERY TYPE of alcohol(including “hard” liquor, wine, and Beer) raisesthe 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 , betacarotene is a precursor of vitamin A andvitamin A has been linked to oral cancer.• Adequate consumption of raw vegetables andfresh fruits gives a lower risk of oral andpharyngeal cancer.• Mechanism: Atrophy of oral mucosamembrane.• This render them more susceptible tocarcinogens.
ULTRAVIOLET LIGHT• Causes– Basal cell carcinoma of the skin– carcinoma of the vermilion border of the lipsespecially in people with outdoor occupation.• Affects men more.
FUNGAL INFECTION• Candida albicans has been implicated in oralsquamous cell carcinoma.• Also found in oral red and white patches withmalignant potentials.• Mechanisms– Production of enzymes which produce genotoxicmetabolites– Its hyphae carrying oncogenes like Ras
VIRAL INFECTION• Human papilloma virus types 16 and 18• Epstein Barr virus (naso-pharyngealcarcinoma)
HABITS• Chewing of betel quids and areca nuts,especially when mixed with tobacco increasesthe risk of developing oral cancer.• Areca has been associated with thedevelopment of Submucous fibrosis• Use of clay pipe has been associated with lipcancer (thermal irritation)
CHRONIC IRRITATION• It is possible that chronic trauma, in additionto other carcinogens, may promote thetransformation of epithelial cells.• Dental calculus, ill fitting dentures, jaggededges of restorations may play a role inlocalizing the site of tumor development.
IMMUNE DEFICIENCY/SUPPRESSION• It could b drug induced or as a result of HIVinfection which could render patientssusceptible to oncogenic viruses• However a definite relationship betweenimmune suppression and oral cancer is yet tobe established.
OCCUPATIONAL RISK• Plays a minor role• Exposure to the following have been associatedwith oropharyngeal and laryngeal cancer;– Cement– Coal products– Wood dust– Organic chemicals– Nickel dust• Occupational exposure to Ultraviolet rays fromsunlight has been associated with cancer of thelips
DIAGNOSIS• Diagnosis of oral cancer and precancer dependson the medical and dental history and clinicalexamination supplemented by investigations• Any chronic oral lesion should be regarded withsuspicion especially in an older patient orassociated with any of the precancerous lesionsand conditions outlined below• Extra caution must also be taken if lesion isindurated, fixed, attached to the underlyingtissue, associated with lymphadenopathy.
Prognostic factors• Tumor size: <2cm• Depth of infiltration: <5mm• Site : lips > oral cavity > oropharynx• Lymph nodes: presence of clinically positive orfixed lymph nodes gives worse prognosis
PREVENTION.• Prevention involves interventions aimed ateliminating, eradicating or minimizing theimpact of the disease• PRIMORDIAL• Avoid the emergence and establishment of thepatterns of living that are known to contribute toan elevated risk of disease
• PRIMARY: Reduce the incidence of cancer andprecancer.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 workersinvolved with chemicals and metals– Health education
PREVENTION.• SECONDARY: aimed at detection of cancer atan early stage• Early detection, especially at theprecancerous stage, offers a better prognosiswith a better chance of cure.› Public education on early signs and selfexamination› Screening
PREVENTION.• TERTIARY: Treat late stage of disease andcomplications
MANAGEMENT• Pre-malignant lesions (precancer)– Management of pre-malignant lesions is guidedfor the most part, by the degree of dysplasiapresent irrespective of clinical appearance.– Dysplasia (mild, moderate, severe)– Non-intervention and intervention strategies maybe adopted depending on the degree of dysplasia.
Non-intervention strategies• Patients with histologic ally proven mild ormoderate dysplastic lesion may be placed on“non-intervention follow-up” in which casethe patient is reviewed regularly every 3-6months and carefully examined for anychanges in the lesion which would necessitateany further biopsy• If the lesion appears clinically unchanged, itshould still be necessary to perform a repeatbiopsy no longer than 3yrs after the initialbiopsy
• Throughout the period of review, repeatattempts at candida isolation andvenopuncture should be undertaken to ensurethat infection or nutritional deficiency has notdeveloped and advice should be given inrelation 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 theexperience of clinician as well as the facilitiesavailable at the treatment centre
MALIGNANT LESIONS (oral caner)• For many years, surgery and/or radiotherapyhas been used as a curative modality• The aim of treatment depends on the stage ofpresentation– Early lesions: can completely be treated by surgeryor radiotherapy.– Late lesions: a palliative treatment is advocated.This could be in the form of radiotherapy, surgeryor both.
• Rehabilitation of patient after surgery couldbe either surgical reconstruction, prostheticreconstruction or both.• This is aimed at restoring esthetics, functionand speech.• All patients must be placed on life-long reviewof about 6monthly intervals during which riskfactors should be continually assessed.
CONCLUSION• In developing countries, including Nigeria,where resources are severely limited,preventive measures should take priority inthe management and control of oral cancer.• Detailed oral examination directed atidentifying precancerous lesions must alwaysbe part of routine medical and dentalexaminations particularly in patients abovethe age of 35yrs
• It is also necessary that all dental and medicalpractitioners should be familiar with the signsand symptoms of oral precancer and cancerbecause this would enhance early diagnosiswhich is very crucial in the management ofthis disease.