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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

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
Q

What is field change in oral cancer?

A

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

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26
Q

Define precancerous lesions/potentially malignant

A

A morphologically altered tissue in which cancer is more likely to occur than in its apparently normal counterpart
= Preferred term is now “potentially malignant”

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27
Q

Name the 2 types of lesions

A

Leukoplakia

Erythroplakia

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28
Q

Leukoplakia WHO definition?

A

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

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29
Q

Epidemiology of leukoplakia?

A

0.9-26.9%
Depends on size of study and population studied
Woldwide prevalence - 2.6%
In UK - 2.8%

30
Q

Homogenous leukoplakia - what does it look like?

A

Flat and plaque like, uniformly white

UNIFORM in colour (white) = lots of keratin on surface and texture

31
Q

Non-homogenous leukoplakia features?

A

Variation in colour and texture - NOT uniform

Also includes: speckled (can have a red background with white speckles), exophytic nodular, verruciform

32
Q

What percentage of leukoplakias becomes malignant in 5yrs?

A

5% become malignant in 5 yrs

  • Homogeneous 1-5%
  • Non-homogeneous 20%
33
Q

Indicators of malignant potential with leukoplakia?

A 
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
Q

Erythroplakia WHO definition?

A

A red patch on the oral mucosa which cannot be characterised clinically or histologically as due to any other condition

35
Q

Erythroplakia features?

A

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
Q

Leukoplakia histology?

A 
Ranges from:
Hyperkeratosis with no dysplasia
Hyperkeratosis with dysplasia
- Mild, mod, severe
Can already be cancerous: Carcinoma-in-Situ or SSC
37
Q

What is epithelial dysplasia?

A

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
Q

What are you looking at in the epithelium regarding atypia dysplasia?

A

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
Q

Mild dysplasia features?

A

Architecture: Changes in lower 3rd
Cytology: mild atypia

40
Q

Moderate dysplasia?

A

Changes into middle 3rd - looks jumbled, cells look darker, bumpy rete processes
Moderate atypia

41
Q

Severe dysplasia?

A

Changes in upper 3rd - almost the full thickness of the epithelium
Severe atypia and numerous mitoses, abnormally high

42
Q

Carcinoma in situ (term not used much any more) features?

A 
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
Q

What percentage of leukoplakias show dysplasia on biopsy?

A

20-50% may show dysplasia on biopsy

  • Homogeneous 20%
  • Non-homogeneous 50%
44
Q

What percentage of dysplastic lesions progress to malignancy, regress, no change or increase in size?

A

Progress to malignancy - 20%
Regress - 20%
No change - 40%
Increase in size - 20%

45
Q

High risk sites?

A

Lateral margins of tongue
Floor of mouth
Retromolar, soft palate and fauces

46
Q

Low risk sites?

A

Gingiva
Buccal mucosa
Labial mucosa
Hard palate

47
Q

How to manage potentially malignant lesions?

A
  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
Q

Techniques/technology in diagnosis and prediction?

A

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
Q

Potentially malignant conditions examples?

A

A generalised state associated with a significantly increased risk of cancer

Chronic hyperplastic candidosis
Actinic keratosis
Submucous fibrosis
Lichen planus

50
Q

Presentation of chronic hyperplastic candidosis?

A 
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
Q

How to treat chronic hyperplastic candidosis?

A

Treat candida

Assess lesion - if still concerned then rebiopsy it

52
Q

Oral submucous fibrosis?

A

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
Q

Oral submucous fibrosis histology?

A

Atrophic with atypia

Fibrosis

54
Q

Oral lichen planus?

A

Lateral border of tongue common
White and red patches
May have matching lesion on other side

55
Q

Symptoms of oral cancer?

A 
None
Soreness/irritation
Paraesthesia/anaesthesia
Disruption of function - Can they move their tongue? Swallow?
Dysphagia
56
Q

Signs of oral cancer?

A 
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
Q

What percentage of oral cancers are in the high risk sites?

A

80%

58
Q

Where to take a biopsy from?

A

The most worrying area
Some normal mucosa next to it
Biopsy is deep enough so you can see it’s full thickness

59
Q

Types of oral cancer?

A

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
Q

Grading of oral cancer - why?

A

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
Q

Staging of oral cancer?

A

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
Q

Effects of previous radiation?

A

Recurrence most frequent route through alveolar crest
Often multiple points of entry wherever tumour near bone
Extensive spread within bone = very aggressive tumour

63
Q

What percentage of pts will have metastases to regional lymph nodes?

A

50%

64
Q

Signs and symptoms of lymph node metastasis?

A 
Painless enlargement (painful usually from infection)
Rock hard mass
Fixation - indicates tumour has spread from node into surrounding tissues
65
Q

What location of oral SCC is most likely to lead to positive nodes (lymph node metastases)?

A

Vental tongue

66
Q

Extranodal extension of cancer - what is this?

A

Tumour extends out of the node into soft tissues

This decreases survival by 50%

67
Q

Haematogenous spread features?

A

Is a late event
Related to advanced disease and poor prognosis
Most commonly extends to lungs

68
Q

Staging of oral cancer table

A 
If any distant metastases = M1 = stage IVc
NO = no lymphnodes
N1 = lymph node 1 
N2a = 2 lymph nodes
etc
69
Q

Prognosis of oral cancers?

A

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
Q

Management of oral cancer?

A 
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
Q

Management in primary dental care?

A

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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