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Detecting Oral
Cancer
What is cancer?
• Cancer is a loss of growth regulation
– Cells grow when they shouldn’t  tumour
– Cells grow where they shouldn’t 
invasion, metastasis
Cancer is a genetic
disease of somatic cells
• Mutations in specific genes can
cause a normal cell to become
cancerous
What are these genes that
lead to cancer when
mutated?
• Proto-Oncogenes
– Gas pedal for cell proliferation
– Mutation  Oncogene  Gas pedal stuck down
• Tumour suppressor genes
– Brakes for cell division
– Mutation  Brakes don’t work
• Care taking (DNA repair) genes
Carcinogenesis
• Carcinogensis is a multistep process
involving mutation in multiple genes
Angiogenesis
• Without blood supply tumour can grow 2mm (106 cells)
• Produce growth factors to stimulate angiogenesis
• Blood vessels around tumour is a bad sign!
Cancer is a loss of growth
regulation induced by:
• Environmental factors
• Genetic factors
Oral Cancer-Introduction
• The 6th most common malignancy within the EC
although the 3rd in men (4th in women) of
developing countries
• The most common malignant tumour in south
east asia.
• 40% of all malignancies in parts of India
• Commoner in males
Introduction
• The prognosis for cure improves the
earlier the diagnosis is made and
appropriate treatment started
• treatment for a small early lesion is
likely to be less mutilating and have a
lower morbidity than treatment for a
large advanced lesion
Introduction
Unlike many malignant lesions
occurring elsewhere in the body
oral scc can be readily observed
in its early stages. There are few
places in the oral cavity that a
lesion can genuinely progress
unnoticed by patient and clinician.
Introduction
The fact that so many patients still
continue to present late with
advanced disease is a sad
indictment of the state of medical
and dental care in the UK!
Incidence and Survival
of Oral or Pharyngeal Cancer
• 5410 new cases diagnosed yearly
– Males 3594
– Females 1816
• 5 year survival rate: 50%
UK 2007
Epidemiology
Squamous cell carcinoma (scc)
accounts for about 90% of all oral
malignancy the remainder include
salivary gland neoplasms,
lymphomas and sarcomas.
Epidemiology
The rate of new oral cancers would
appear to be falling from its peak in
1920 to the present levels. However,
there is disturbing evidence that
cancers of all types including oral
cancer are on the increase.
Epidemiology
• there is a strong clinical impression
as yet unsubstantiated that we are
seeing a rise in incidence of
aggressive oral scc in young patients
with no accepted risk factors
Aetiology
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Smoking
Chewing habits
Alcohol
Poor diet
Industrial hazards
Dental factors
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Actinic Radiation
Epithelial atrophy
Viruses
Immunosuppression
Candida infection
Aetiology
• Smoking:
Cigar and pipe smoking Vs cigarette smoking
Reverse smoking
• Chewing habits:
Pan chewing → Leukoplakia → SCC
• Alcohol:
Unclear mechanism
Type and quality more important than quantity
Aetiology
Smoking and Alcohol synergism
• Smoking alone: 9 times greater risk
• Alcohol alone: 8 times greater risk
• Smoking and alcohol consumption:
9+8=40!!
Aetiology
• Industrial hazards:
Higher incidence in textile workers
• Dental factors
• Actinic Radiation:
SCC more common in lower lip than upper lip
Lip cancer is rare in dark-skinned people
• Epithelial atrophy:
May enhance the absorption of carcinogens
Aetiology
• Viruses:
HPV particularly types 16 & 18
• Immunosuppression:
Increased incidence of certain cancers in
patients with renal transplants or HIV
• Candidal infection:
Chronic hyperplastic candidosis is premalignant
Your average oral SCC patient!
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Male with carious teeth
Rarely attends dentist!!!!!!
Smokes 40-60 since ???
Drinks cheap alcohol
Eats “junk food” on the road whilst
running around in his delivery van!
Indications for urgent referral
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Any unhealed ulcer for more than two weeks
Any unexplained oral bleeding
Any area of induration
Any unexplained white patch
All-red or red/white patches
Cervical nodes
Clinical presentation
• Can affect any part of the oral mucosa
• Sites particularly at risk vary according to
aetiological factors:
Europe: Tongue and lip
India: Buccal mucosa
Clinical presentation
• Early lesions are usually asymptomatic
• May present as:
a white patch
a red patch
an ulcer
an exophytic growth
Clinical presentation
• Pain may be a late feature
• Advanced lesions have a very variable
presentation
• Bone destruction may be evident on
radiographs
• Teeth may become mobile
• There may be altered sensation
Our Role
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Patient education
Elimination of risk factors
Thorough examination
Be safe.. refer if in doubt
Examination Overview
• Head and neck exam should be a routine
part of dental and medical check-ups.
• Take a history of alcohol and tobacco use.
• Follow up on suspicious signs.
Tools and Time
• Proper lighting
• Dental mouth mirror
• Gauze squares
• Gloves
• 5 minutes
Oral Lesions Suspicious
for Oral Cancer
• Homogenous leukoplakia
• Leukoplakia with early squamous cell
carcinoma
• Nodular leukoplakia with severe epithelial
dysplasia
• Erythroleukoplakia with candida infection
Leukoplakia
• Idiopathic white patch that cannot be wiped off the
mucosa
• Up to 4% risk of malignant change in 5 years
• Very variable clinical presentation (homogeneous,
speckled, verrucous, nodular,..etc)
• Management include biopsy, conservative treatment,
excision, and laser ablation
Erythroplasia (erythroplakia)
• Red velvety patches
• Idiopathic
• Very high risk of
malignant change
• 70% are carcinomas
in situ on first biopsy
• Same management as leukoplakias
Candidal leukoplakia
• Rough adherent
white plaque
• Typical site is buccal
mucosa behind the
commissures
• Variable risk of malignant change
• Management is with vigorous systemic
antifungals
Lichen planus
• Chronic inflammatory mucocutaneous
disease
• Unclear pathogenesis
• Two distinctive clinical types
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(non-erosive and erosive)
• Usually bilateral distribution
• Only erosive type is premalignant
• Management includes biopsy and
steroids
Epithelial dysplasia
• Loss of tissue architecture
• The degree of dysplasia is widely believed
to be an important factor but there is little
definitive evidence to support this
assertion
Early stages may be reversible !
Precancerous lesions
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Risk of malignant transformation depends on:
1. Site
2. Nature of lesion
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Can’t predict if the lesion will
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Regress (15%)
Remain the same
Progress to cancer (4-8%)
Management of precancerous
lesions
• Remove the apparent cause if possible
(stop smoking, antifungals)
• Biopsy
• Long term review
Prognosis of oral cancer
STNMP system:
Site
Tumour size
Node involvement
Metastasis
Pathology
Staging
• T1 <2cm. T2 >2cm<4cm. T3 >4cm.
T4 massive tumour with invasion
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N0: No nodes
N1: ipsilateral <3cm
N2a: ipsilateral >3cm<6cm
N2b: ipsilateral multiple <6cm
N2c: Bilateral/Contralateral: <6cm
N3: any node >6cm
Investigation
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Surgical biopsy, Incisional
FNA, for neck and parotid lumps
Radiographs
CT
Ultrasound esp for abdomen and liver
mets.
Treatment
• CURATIVE
• LOCAL DISEASE CONTROL
• PALIATIVE ONLY
Team Approach
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Maxillofacial Surgeon
Plastic/Neuro surgery
Oncologist
Radiotherapist
Nutritionist
Speech therapist
Dentist
Maxillofacial prosthodontist
Treatment
Treatment modalities:
• Surgical excision
• Radiotherapy
• Chemotherapy??
• Surgery and radiotherapy
Surgery
• Excision of the tumour with a safety
margin
• 1-2cm 3D margin for SCC
• Intra-bony lesions require bigger
margin
• Partial mandibulectomy or
maxillectomy with soft tissue and
L.Ns
Management of the neck
• Therapeutic neck dissection: When
disease is obviously present in the neck
and the dissection is undertaken to ablate
the disease
• Elective neck dissection; No obvious
clinical disease in the neck but a high
chance of occult disease or neck opened
for access
Early Detection Saves
Lives!
• 5-year survival for localized disease is
76%
• 5-year survival for metastatic disease is
19%
Radiation mucositis
• Generalized erythematous and ulcerative response
of oral mucosa
• Starts the 2nd week of treatment with radiotherapy
• Very painful
• Secondary infection worsen the condition
• subsides after the course of radiation leaving
atrophic epithelium and avascular submucosa
Treatment of radiation
mucositis
• Sodium bicarbonate & camomile mouth-wash
• Benzydamine hydrochloride MW (anti-inflammatory,
anti-microbial, analgesic)
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Miconazole for candidosis
Soft diet
Artificial saliva may help
PTA (polymyxin E, tobramycin, amphotericin) lozenges
(reduces duration and severity)
Osteoradionecrosis
• Radiation affects the vascularity of bone 
more susceptible to infection
• Painful necrosis with sloughing of overlying
soft tissues
• Extraction with antibiotic cover
• ORN is more likely if extraction after a long
period of radiotherapy treatment
Dental practitioner role
1. Early detection of suspicious lesions
2. Prevention (e.g. stop smoking advice)
3. Prophylactic treatment before radiotherapy
4. Lifelong monitoring after radiotherapy
5. Prostho. treatment as part of reconstruction