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Oral Disease > Aetiology, epidemiology, clinical and pathological features of oral cancer > Flashcards

Aetiology, epidemiology, clinical and pathological features of oral cancer Flashcards

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1
Q

What does oral cancer involve and not involve?

A

The oropharynx but NOT the salivary glands

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2
Q

Epidemics of oral cancer?

A 
16th most common cancer worldwide 
Head and neck = 6th most common
Cases - 355,000
Males: 5.8/100,000
Females: 2.3/100,000
Deaths 177000
Death rate 50%
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3
Q

Where is oral cancer most common?

A

Sri-Lanka

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4
Q

Oral cancer in England?

A

Cases: 7587 including the pharynx
4379 true oral cavity

3% of all cancers
Males: 20.1/100,000
Females: 9.3/100,000

Deaths 2427
5yr survival 58%

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5
Q

Are oral cancer deaths increasing or decreasing/

A

Increasing

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6
Q

Problems with oral cancer?

A

Increasing incidence
Younger patients
Little improvement in survival - only a modest increase in survival in 50yrs

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7
Q

Who does oral cancer most commonly affect?

A

A disease of older men typically - 60s and 70s - heavy smoker
But now more women have it and it is more common in younger populations - 40-49 yr olds

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8
Q

Why is the oral cancer death rate so high?

A

Pt’s present late so survival is poor

Stage III and stage IV presentation = late/advanced stage disease

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9
Q

The location of the cancer can vary the survival rate, list the highest to lowest survival rates per location

A 
Lip = high 5 yr survival rate
Oral cavity
Tongue
Oropharynx
Hypotharynx = Lowest
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10
Q

Aetiology of oral cancer?

A

Multifactorial:

  • No single factor identified
  • Genetic predisposition in some (rare)
  • Environmental

Factors vary in different locations and ethnic groups

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11
Q

Inherited factors in oral cancer?

A

Polymorphisms in genes involved in the metabolism of carcinogens have been linked to individual susceptibility:

  • Tobacco - glutathione transferases = carcinogens stay for longer than they should
  • Alcohol - Alcohol dehydrogenase (ALDH2)

An increased risk of oral cancer is associated with a number of inherited cancer syndromes:

  • Li-fraumeni - abnormal P53
  • Fanconi anaemia
  • Xeroderma pigmentosum
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12
Q

Risk factors for oral cancer?

A 
Tobacco
Alcohol
Sunlight
Infections 
- Viruses (human papilloma virus) 
- Fungi (chronic hyperplastic candidosis has a 25% risk of becoming malignant) 
- Bacteria
Diet and nutrition
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13
Q

What tobacco use can cause oral cancer?

A

Smoking tobacco

  • Cigarettes
  • Pipes
  • Cigars
  • Reverse smoking
  • Definite relationship with oral cancer
  • Risk is greatest in heavy users >20/day
  • Risk is greater if accompanied by alcohol use

Smokeless tobacco

  • Betal quid (paan)
  • Snuff
  • Chewing tobacco
  • Definite relationship with oral cancer established by epidemiological studies, observation of lesions
  • Risk is greatest in heavy users
  • Risk is greater if with smoking or alcohol
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14
Q

Areca/betal nut/paan chewing features?

A

Used as a stimulant
Common in SE Asia
Stains teeth and linked with oral cancer

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15
Q

Alcohol as a risk factor of oral cancer?

A

Risk factor of oral cancer

  • Ethanol alone is not carcinogenic
  • Amount of ethanol more important than type

Risk is greatest with tobacco
Increasing importance in young pts

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16
Q

Recommended units of alcohol per week?

A

14 units per week for men and women
= 6 pints of beer
= 7 glasses of wine
= 14 shots of spirit

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17
Q

What can UV cause?

A

Lip (skin) cancer (BCC, mostly SCC, melanoma)

UV light causes solar keratosis and dysplasia of the skin

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18
Q

Viruses causing oral cancer?

A 
HPV
Good evidence for role in oropharynx 
- Some evidence in oral lesions 
HPV 16 and 18 have been implicated
HPV associated with about 60% of OPSCC cases in UK
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19
Q

HPV related oropharyngeal SCC features?

A

Younger pt demographic
- Less traditional risk factors (pt’s who do not smoke)
Often present with LN metastases - may not see it in mouth (lymph node exam and ask if pt noticed any lumps)
Prognosis is good (chemoradiotherapy)
- Advantage lost is also a smoker
Effects of vaccination of HPV vaccine will hopefully reduce or eventually irradicate this cancer

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20
Q

Histology of HPV-OPSCC?

A

p16 marker is used as a surrogate for HPV infection

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21
Q

Candida and oral cancer?

A

Candida infection has an association with oral cancer development
Evidence:
- Candida can produce carcinogens from nicotine and alcohol
- Candida often infect pre-malignant lesions
- Candida leukoplakia (CHC) is often non-homogenous and dysplastic

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22
Q

Social deprivation and oral cancer?

A

More deprived = most likely to have cancer

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23
Q

Oral cancer genetics?

A

Oncogenes

  • Differing oncogenes activated
  • Geographical variations
  • No clear relationship with disease

Tumour suppressor genes
- p53 mutation or inactivation - linked to HPV

Viral component - what role does HPV play in OSCC?

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24
Q

Multistage carcinogenesis of oral cancer?

A

Initiation (Normal cell) - Induction when multiple genetic events occur (due to inherited and environmental factors) - causes pre-cancer cells
Progression - multiple genetic events = cancer cells

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25
What is field change in oral cancer?
All/most of the oral mucosa is abnormal - but not necessarily clinically or on histology Common genetic abnormalities Subsequent tumours may develop in the field of abnormal mucosa or may be completely different = If you treat just the lesion you can see, you may leave behind an area of abnormal epi = develop another lesion
26
Define precancerous lesions/potentially malignant
A morphologically altered tissue in which cancer is more likely to occur than in its apparently normal counterpart = Preferred term is now "potentially malignant"
27
Name the 2 types of lesions
Leukoplakia | Erythroplakia
28
Leukoplakia WHO definition?
A white patch that cannot be rubbed off and cannot be characterised clinically or histologically as another other disease... ...and that is not associated with any physical or chemical causative agent except the use of tobacco If can be rubbed off - probs candida
29
Epidemiology of leukoplakia?
0.9-26.9% Depends on size of study and population studied Woldwide prevalence - 2.6% In UK - 2.8%
30
Homogenous leukoplakia - what does it look like?
Flat and plaque like, uniformly white | UNIFORM in colour (white) = lots of keratin on surface and texture
31
Non-homogenous leukoplakia features?
Variation in colour and texture - NOT uniform | Also includes: speckled (can have a red background with white speckles), exophytic nodular, verruciform
32
What percentage of leukoplakias becomes malignant in 5yrs?
5% become malignant in 5 yrs - Homogeneous 1-5% - Non-homogeneous 20%
33
Indicators of malignant potential with leukoplakia?
``` Site - high risk: - Floor of mouth - Ventral of tongue - Lateral borders of tongue - Anterior papilla of the tonsil Colour - RED areas in a lesion Texture - variations in thickness have higher risks of progression Presence of candida - higher risk Degree of dysplasia ```
34
Erythroplakia WHO definition?
A red patch on the oral mucosa which cannot be characterised clinically or histologically as due to any other condition
35
Erythroplakia features?
Use of term varies (erosive/specked lesion) Prevalence unknown but less than leukoplakia Has a higher malignant potential than leukoplakia Often shows severe dysplasia or CiS May be the earliest clinical sign of invasive SCC
36
Leukoplakia histology?
``` Ranges from: Hyperkeratosis with no dysplasia Hyperkeratosis with dysplasia - Mild, mod, severe Can already be cancerous: Carcinoma-in-Situ or SSC ```
37
What is epithelial dysplasia?
A collective term used to embrace a number of individual atypical features Graded as mild/mod/severe on extent/degree of atypical features - subjective A premalignant-state with an increased risk of cancer development Severe dysplasia involving the full epithelial thickness = carcinoma in situ
38
What are you looking at in the epithelium regarding atypia dysplasia?
Architectural features: - Irregular epithelial stratification - Loss of basal cell polarity - Drop shaped rete processes Cytological features - Increased number of mitotic figures - Cellular and nuclear pleomorphism - Nuclear hyperchromatism - Individual cell keratinisation - Loss of intercellular adherence
39
Mild dysplasia features?
Architecture: Changes in lower 3rd Cytology: mild atypia
40
Moderate dysplasia?
Changes into middle 3rd - looks jumbled, cells look darker, bumpy rete processes Moderate atypia
41
Severe dysplasia?
Changes in upper 3rd - almost the full thickness of the epithelium Severe atypia and numerous mitoses, abnormally high
42
Carcinoma in situ (term not used much any more) features?
``` Malignant but not invasive Abnormal architecture - Full thickness of viable cell layers Pronounced cytological atypia - Mitotic abnormalities frequent ``` Looks like cancer but cannot see invasion
43
What percentage of leukoplakias show dysplasia on biopsy?
20-50% may show dysplasia on biopsy - Homogeneous 20% - Non-homogeneous 50%
44
What percentage of dysplastic lesions progress to malignancy, regress, no change or increase in size?
Progress to malignancy - 20% Regress - 20% No change - 40% Increase in size - 20%
45
High risk sites?
Lateral margins of tongue Floor of mouth Retromolar, soft palate and fauces
46
Low risk sites?
Gingiva Buccal mucosa Labial mucosa Hard palate
47
How to manage potentially malignant lesions?
1. Systemic examination - Screening tools: 2. Provisional clinical diagnosis 3. Biopsy 4. Definable lesion - manage accordingly - Eliminate possible cause (good response - definable lesion - manage accordingly OR no response = no definable lesion - dysplasia or no dysplasia = tx, observation and follow up - No obvious cause - no definable lesion, dysplasia or no dysplasia = tx, observation, follow up
48
Techniques/technology in diagnosis and prediction?
A thorough and systemic examination Mucosal stains e.g. Toluidene blue Imaging systems Brush biopsy - cytology assessment, lab-on-a-chip (uncomfortable - may as well take biopsy) DNA image cytometry OraScreen stains abnormal epithelium blue (but lots of other lesions stain blue e.g. lichen planus) VELscope - light on normal mucosa, not on abnormal mucosa Z-scan = passes electrical current into tissue - how it passes the tissue tells you about its structure - used routinely
49
Potentially malignant conditions examples?
A generalised state associated with a significantly increased risk of cancer Chronic hyperplastic candidosis Actinic keratosis Submucous fibrosis Lichen planus
50
Presentation of chronic hyperplastic candidosis?
``` Present at angles of mouth Can be white patch or mixed red and white patch Well defined Pre-malignant Candida hyphae purple in histology ```
51
How to treat chronic hyperplastic candidosis?
Treat candida | Assess lesion - if still concerned then rebiopsy it
52
Oral submucous fibrosis?
Predominantly seen in Indians and Asians Associated with areca nut use (paan) Precise mechanism uncertain Once develops no regression and no effective tx Risk of malignant transformation 2.3-7.6% 1st stage = fibrosis of oral mucosa, blanches when stretched 2nd stage = red and white patches on mucosa, cannot open mouth much, brown stains on teeth, buccal mucosa rigid and hard to touch
53
Oral submucous fibrosis histology?
Atrophic with atypia | Fibrosis
54
Oral lichen planus?
Lateral border of tongue common White and red patches May have matching lesion on other side
55
Symptoms of oral cancer?
``` None Soreness/irritation Paraesthesia/anaesthesia Disruption of function - Can they move their tongue? Swallow? Dysphagia ```
56
Signs of oral cancer?
``` Persistent ulcer Persistent white, red or mixed patch Exophytic mass Fixation of tissue Induration Firmness Sensory/motor deficit Tooth movement/mobility Lymph node enlargement/fixation ```
57
What percentage of oral cancers are in the high risk sites?
80%
58
Where to take a biopsy from?
The most worrying area Some normal mucosa next to it Biopsy is deep enough so you can see it's full thickness
59
Types of oral cancer?
Squamous cell carcinoma - majority Verrucous carcinoma - Relatively low grade - Rarely metastasises - Tobacco/snuff use - Exophytic surface - Will gradually cover more and more of the oral surface - Pushing invasive pattern Others - both very aggressive - Basaloid - Spindle cell
60
Grading of oral cancer - why?
Gives an indication of prognosis Helps differentiate tumours that may do well from tumours that may not Done by the pathologist on biopsies Well differentiated: - Resembles cell of origin - Expresses keratins Moderately differentiation - Majority - Little bit of keratinisation - Invading into underlying muscle - Resembles cell of origin Poorly differentiation - Aggressive - No keratin - May not resemble cell of origin (anaplastic) - Necrosis common
61
Staging of oral cancer?
TNM - tumour, nodes, metastases - Local extension of disease - T1-4 Important features in the primary tumour: - Overall tumour size - Invasion into muscle (tongue) - Involvement of nerves/blood vessels - Invasion into bone - tumour is growing into underlying CT = makes it malignant --- >5mm has a worse prognosis as risk of lymph node metastases increases - Perineural spread - involving small nerves at the advancing edge - extensive spread related to IAN may give RECURRENCE - Tumour in vessels - lymphatics or blood vessels = risk of metastases - Spread to bone: Makes it a T4 tumour - edentulous pts usually into gaps in cortex, in dentate pts via periodontal ligament
62
Effects of previous radiation?
Recurrence most frequent route through alveolar crest Often multiple points of entry wherever tumour near bone Extensive spread within bone = very aggressive tumour
63
What percentage of pts will have metastases to regional lymph nodes?
50%
64
Signs and symptoms of lymph node metastasis?
``` Painless enlargement (painful usually from infection) Rock hard mass Fixation - indicates tumour has spread from node into surrounding tissues ```
65
What location of oral SCC is most likely to lead to positive nodes (lymph node metastases)?
Vental tongue
66
Extranodal extension of cancer - what is this?
Tumour extends out of the node into soft tissues | This decreases survival by 50%
67
Haematogenous spread features?
Is a late event Related to advanced disease and poor prognosis Most commonly extends to lungs
68
Staging of oral cancer table
``` If any distant metastases = M1 = stage IVc NO = no lymphnodes N1 = lymph node 1 N2a = 2 lymph nodes etc ```
69
Prognosis of oral cancers?
Related to - Site - Grade - Stage - Related to size (T) and spread (N and M) - Extracapsular spread - Multiple primaries - 15 to 20% - synchronous or metachronous
70
Management of oral cancer?
``` Confirm/establish diagnosis by biopsy Through clinical examination Imaging for extent of spread - MRI, potential CT of chest or PET scan Review at multidisciplinary team meeting Tx plan formulated: - Surgical excision and/or - Radiotherapy and/or - Chemotherapy - Palliation ```
71
Management in primary dental care?
Do NOT biopsy Prompt referral Refer to local oral and maxillofacial surgery department - 2 week target Do not tell the pt they have cancer Do tell them you are concerned and they should be seen by a specialist

Oral Disease (42 decks)

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