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Oral Disease for FINALS > Oral cancer and precancer > Flashcards

Oral cancer and precancer Flashcards

1
Q

International Classification of Disease (ICD)10 (4)

A

C00-C06, C12-C14

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2
Q

What does ‘oral’ cancer include? (2)

A

Includes oropharynx, but not salivary glands

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3
Q 
How common is oral cancer? 
-what place
-total cases
-frequency
incidence
-deaths
-death rate
A 
16th most common
355,000 cases
2% frequency
5.8/100,000
128,000 deaths*
50% death rate
(H&N is 6th most common worldwide)
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4
Q

Oral Cancer: England stats

A

Total cases: 7587 including pharynx, 4379 true oral cavity
Frequency: 3% of all cancers
Incidence: M 20.1/100,000, F 9.3/100,000
58% 5 year survival

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5
Q

Regional differences: h&N cancer (4)

A

NI < England < Wales < Scotland

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6
Q

Increasing incidence (3)

A

On the rise
Men: 32%increase over last 10 years, now 10th
33% increase in women over last 10 years, now 15th

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7
Q

Age group is changing

A

Still predominantly older men
Now more women, and younger age demographic
Older patients decreasingly affected

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8
Q

Survival rates of H&N cancer: the change over time

A

Not much change over 50 years at all

  • 7% of pts present with late stage disease (stage III or stage IV)
  • in some IO subsites (further back in the oral cavity), >60% of pts die
  • -> survival goes down the further back the lesion as harder to be seen
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9
Q

Aetiology of oral cancer (2)

A

Multifactorial
-no single factor identified
-genetic predisposition in some (pretty rare)
-environmental
Factors vary in different geographical regions or ethnic groups

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10
Q

Inherited factors in oral cancer (2)

A

Polymorphisms in genes involved in the
metabolism of carcinogens have been linked
to individual susceptibility (e.g. in Japan and South Korea):
• tobacco - glutathione transferases
• alcohol - alcohol dehydrogenase (ALDH2)
An increased risk of oral cancer is associated with a number of inherited cancer syndromes (in skin lesions including the lip):
• Li-Fraumeni (abnormal P53)
• Fanconi anaemia (DNA damage repair abnormality - primarily related to bone marrow but if they survive that, 60% of them get oral cancer)
• Xeroderma pigmentosum (DNA damage repair abnormality)

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11
Q

Risk factors for oral cancer (5)

A 
Tobacco
-strongest risk factor
Alcohol
Sunlight
Infections
• Viruses
• Fungi
• Bacteria
Diet and nutrition
Age
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12
Q

Tobacco use: types of use (2)

A 
Smoking 
-cigarettes
-pipes
-cigars
-reverse smoking
Smokeless
-betel quid (pan)
-snuff
-chewing tobacco
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13
Q

Tobacco smoking risk (3)

A 
• definite relationship with
oral cancer
• risk is greatest in heavy
users (>20/day)
• risk is greater if
accompanied by alcohol
use
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14
Q

Smokeless tobacco (3)

A 
Definite relationship with oral cancer
established by:
• epidemiological studies
• observation of lesions - area in contact with tobacco is the area that gets cancer
Risk is greatest in heavy users
Risk is greater if accompanied by
smoking or alcohol
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15
Q

Alcohol as a risk factor (3)

A 
Consumption of alcoholic
drinks is a risk factor for oral
cancer
• ethanol alone is not
carcinogenic
• amount of ethanol more
important than type
Risk is greatest when
accompanied by tobacco use
Increasing importance in
young patients
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16
Q

Sunlight and oral cancer (2)

A 
• UV is an important
cause of lip (skin)
cancer (BCC, SCC,
melanoma)
• UV light cause solar
keratosis and dysplasia
of the skin
-squamous cell carncinomas
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17
Q

Viruses and oral cancer (4)

A 
HPV
• Good evidence for a role in oropharynx
-some evidence in oral lesions
• HPV 6 &amp; 18 have been implicated
• HPV associated with about 60% of OPSCC cases in the UK
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18
Q

HPV-related Oropharyngeal SCC (4)

A 
Younger patient demographic
• less traditional risk factors
Often present with LN metastases
Prognosis is good (chemoradiotherapy)
• “advantage” lost if also a smoker
Effects of vaccination??
-stained with p16 in histology
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19
Q

Evidence about candida and oral cancer (4)

A

Candida infection has an association with oral cancer development
• candida often infects pre-malignant lesions
• candidal leukoplakia is often dysplastic
• candidal leukoplakias are often non-homogeneous
• candida can produce carcinogens from nicotine and alcohol

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20
Q

Oral cancer genetics (3)

A 
Oncogenes
• differing oncogenes activated
• geographical variations
• no clear relationship with disease
Tumour suppressor genes
• p53 mutation or inactivation
• many other genes
Viral component – what role does HPV play?
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21
Q

Social deprivation and oral cancer

A 
Social deprivation has an impact
Highest rates in most deprived males
-smoking
-access to good nutrition
-access to healthcare and related behaviours
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22
Q

Multistage carcinogenesis (3)

A

Inititaion (normal cell) — multiple genetic effects –> induction (precancer) — multiple genetic events –> progression (cancer)
*genetic events due to inherited and environmental factors

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23
Q

Field change (3)

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
“Field of cancerisation”
Need to treat the whole field rather than just the lesion

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24
Q

Stages of cancer development (3)

A

Keratosis –> dysplasia –> carcinoma

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25
Precancerous lesion definition (2)
a morphologically altered tissue in which cancer is more likely to occur than in its apparently normal counterpart The preferred term is now “potentially malignant oral lesion”
26
WHO definition of leukoplakia (2)
WHO definition: A white patch that cannot be rubbed off and cannot be characterised clinically or histologically as any other disease… …and that is not associated with any physical or chemical causative agent except the use of tobacco
27
Epidemiology of leukoplakia (3)
``` No good registration schemes Most “precancer” studies have looked at leukoplakia Prevalence: •Ranges from 0.9% to 26.9% •Depends on size of study and the population studied ```
28
Worldwide prevalence of leukoplakia (1)
2.6%
29
UK prevalence of leukoplakia (1)
2.8%
30
Homogenous leukoplakia (2)
Flat and plaque-like, uniformly white
31
Non-homogenous leukoplakia (2)
Variation in colour or texture nodular, verruciform, exophytic, speckled
32
Erythroplakia WHO definition (1)
a red patch on the oral mucosa which cannot be characterised clinically or histologically as due to any other condition.
33
Erythroplakia (4)
* Use of term varies (erosive/speckled) * Prevalence unknown but << leukoplakia * >> malignant potential than leukoplakia * Often shows severe dysplasia or CiS * Earliest clinical sign of invasive SCC
34
Leukoplakia and malignancy (3)
``` 5% become malignant in 5 years -homogenous 1-5% -non-homogenous 20% Indicators of malignant potential: -site e.g. lateral order of tongue, ventral tongue, floor of mouth, anterior pillar of tonsil onto lateral part of soft palate -colour e.g. red in it -texture e.g. thick areas/ variations in thickness -presence of candida -degree of dysplasia ```
35
Histology of leukoplakia ranges from (4)
``` Hyperkeratosis with no dysplasia Hyperkeratosis with dysplasia • Mild • Moderate • Severe Carcinoma-in-Situ Squamous cell carcinoma ```
36
Dysplasia (4)
• A collective term used to embrace a number of individual atypical features • Graded as mild / moderate / severe on extent/ degree of atypical features – ‘subjective’ • A pre-malignant state with an increased risk of cancer development • Severe dysplasia involving the full epithelial thickness = Carcinoma in Situ
37
Atypia in epithelium: architechtural features (3)
* Irregular epithelial stratification * Loss of basal cell polarity * Drop-shaped rete processes
38
Atypia in epithelium: cytological features (5)
* Increased numbers of mitotic figures * Cellular & nuclear pleomorphism * Nuclear hyperchromatism (‘ploidy’) * Individual cell keratinisation * Loss of intercellular adherence
39
Mild dysplasia histology (2)
Architecture: changes in lower third Cytology: mild atypia
40
Moderate dysplasia histology (2)
Architecture: change into middle third Cytology: moderate atypia
41
Severe dysplasia histology (2)
Architecture: changes in upper third Cytology: severe atypia and numerous mitoses, abnormally high
42
Carcinoma-in-situ (3)
``` Malignant but not invasive Abnormal architecture • full thickness of viable cell layers Pronounced cytological atypia • mitotic abnormalities frequent ```
43
Leukoplakia and dysplasia (3)
20 - 50% may show dysplasia on biopsy: • Homogeneous: 20% • Non-homogeneous:50%
44
Fate of dysplastic lesions (4)
Malignant 20% Regress 20% No change 40% Increase in size 20%
45
Management of potentially malignant lesions : see table
See table
46
Screening techniques (5)
* A thorough & systematic examination!! * OraScreenTM (Toluidene blue) - blue stain on cancer but so do lots of other oral lesions! Not specific so not used routinely * Exfoliative cytology * Brush biopsy (Cytobrush) * DNA image cytometry – the future? * Velscope blue excitation light - green fluorescence on normal tissue, none on abnormal
47
Exfoliative cytology (4)
* Wooden spatula * Surface scraping onto slide + stain * Keratin surface complicates * May miss dysplastic/malignant cells
48
Brush biopsy (3)
A technique for sampling cells of a lesion Atypical and malignant cells are found in the basal layers -cells from all layers including the basal are sampled
49
Potentially malignant conditions (5)
a generalised state associated with a significantly increased risk of cancer - chronic hyperplastic candidosis - actinic keratosis - submucous fibrosis - lichen planus
50
Oral submucous fibrosis histology (2)
Atrophic witha typia | Fibrosis
51
Clinical features of oral cancer: symptoms (5)
``` • None • Soreness/ irritation • Paraesthesia/ anaesthesia • Disruption of function • Dysphagia ```
52
Clinical features of oral cancer: signs (8)
``` • persistent ulcer • persistent white, red or mixed patch • exophytic mass • fixation of tissue • induration • sensory/motor deficit • tooth movement/mobility • lymph node enlargement/fixation ```
53
High risk sites (8)
``` • Floor of Mouth • Lateral border of tongue • Retromolar region -these three make up 80% • Soft palate and fauces • Gingiva • Buccal mucosa • Labial mucosa • Hard palate ```
54
Types of oral cancer (4)
Squamous cell carcinoma Verrucous carcinoma Basaloid Spindle cell
55
Verrucous carcinoma (5)
* relatively low grade * rarely metastasises * tobacco/snuff use * exophytic surface * ‘pushing’ invasive pattern
56
Grade (3)
* Grading gives an indication of prognosis * Helps differentiate tumours that may do well from tumours that may not * Grading is done by the pathologist on biopsies
57
Erythroplakia malignant
25% will already be malignant upon diagnosis
58
Stage: spread of oral cancer
``` Local extension of disease varies according to site -mucosal extension -muscle (tongue etc.) -bone -nerve -influence of previous radiotherapy TNM staging ```
59
Depth of invasion (1)
>5mm has a worse prognosis
60
Perineural spread (2)
Involving small nerves at the advancing edge | Extensive spread related to inferior alveolar nerve may give recurrence
61
Spread to bone (2)
Edentulous: gaps in cortex Dentate: via PDL -becomes a T4 tumour
62
Effect of previous irradiation (3)
* most frequent route through alveolar crest * often multiple points of entry wherever tumour near bone * extensive spread within bone
63
Mestastases stats (1)
50% of pts will have matastases to regional lymph nodes
64
Signs and symptoms of lymph node metastasis (3)
• Painless enlargement • “Rock hard” mass • Fixation- indicates tumour has spread from node into surrounding tissues
65
How does tumour enter lymph node (1)
By subcapsular sinus via afferent lymphatics
66
Extracapsular spread (2)
Tumour extends out of the node into soft tissue | ECS decreases survival by 50%
67
Haematogenous spread (3)
``` Haematogenous spread is a late event Related to -advanced disease -poor prognosis Most commonly to lungs ```

Oral Disease for FINALS (34 decks)

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