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FINALS - Oral Medicine > Oral Cancer > Flashcards

Oral Cancer Flashcards

1
Q

What are the two patterns of oral cancer?

A

Oral cavity cancer
Oro-pharyngeal cancer

Each have their own populations, outcomes, and risks.

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2
Q

What is the estimated incidence of oral cavity cancer in the world population?

A

2.5 per 100,000

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3
Q

Who is at greater risk of developing oral cavity cancer?

A

Males more than females (2:1)
Smokers
Alcohol users
Lower socioeconomic status
Poor diet

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4
Q

By what factor do smokers increase their risk of oral cancer?

A

2 times

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5
Q

By what factor do drinkers (3-4/day) increase their risk of oral cancer?

A

2 times

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6
Q

By what factor do those who smoke and drink increase their risk of oral cancer?

A

5 times

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7
Q

What is happening to the rate of incidence of worldwide oral cavity cancer?

A

Decreasing in men, increasing in women, likely due to the reduction in tobacco use.

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8
Q

What is the estimated incidence of oro-pharyngeal cancer?

A

1.4 per 100,000
Male 4.8:1 Female
Generally increasing rates.

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9
Q

What impact does diet and health have to oral cancer risk?

A

There is limited data to support dietary factors such as low intake of fresh fruit/veg increases risk.

There is no known associated risk with obesity.

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10
Q

Why might socioeconomic status increase risk of oral cancer?

A

May be cause of smoking/drinking

Could also be lower education in population.

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11
Q

What is meant by the term dysplasia?

A

Dysplasia refers to the abnormal development of cells within tissues or organs. It can lead to various conditions that involve enlarged tissue, such as hip dysplasia.

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12
Q

What is meant by the term potentially malignant lesions?

A

Lesions that are en route to becoming cancer, much more likely to become cancer, or potentially malignant.

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13
Q

Which types of lesion are potentially malignant?

A

White lesions (leukoplakia)
Red lesions (erythroplakia)
Lichen planus
Oral submucous fibrosis

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14
Q

How would you identify a potentially malignant leukoplakia?

A

White patch does not rub off
Not linked to any other disease

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15
Q

How would you identify a potentially malignant erythroplakia?

A

Red lesion
Not linked to any other disease

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16
Q

What % of leukoplakia turn out to be malignant?

A

0.2-4% depending on timeframe

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17
Q

Which carries the higher dysplasia risk, erthyroplakia or leukoplakia?

A

Erythroplakia have a greater dysplasia risk, with around 50% of lesions already being a carcinoma.

However they occur much less frequently than leukoplakia.

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18
Q

How do you determine dysplasia of tissues?

A

Cellular atypia
Epithelial architectural organisation

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19
Q

How can dysplasia be categorised?

A

Low grade
High grade
Carcinoma-in-situ

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20
Q

What cytological cell changes can be seen in tissues with dysplasia?

A

Abnormal variation in:

Nuclear shape
Nuclear size
Cell size
Cell shape
Nuclear-cytoplasmic ratio

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21
Q

What architectural changes may be seen in tissues with dysplasia?

A

Irregular stratification
Loss of polarity of basal cells
Drop shaped rete ridges
Abnormal keratinisation
Loss of cell cohesion
Keratin pearls within rete ridges

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22
Q

What constitutes low-grade mucosal dysplasia?

A

Easily identifiable tumour
Considerable amount of keratin
Evidence of stratification
Well formed basal layer

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23
Q

What constitutes high-grade mucosal dysplasia?

A

Little resemblance to normal epithelium
Considerable atypia
Invade pattern with fine cords

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24
Q

What is carcinoma-in-situ?

A

A theoretical concept
Cytologically malignant but non-invading
Abnormal architecture

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25
What is squamous cell carcinoma?
Carcinoma starting in the squamous cells of an epithelium.
26
Which histological factors can be used to indicate prognosis of an oral cancer patient?
Pattern of invasion Depth of invasion Perineural invasion Invasion of vessels
27
What is the field cancerisation concept?
There is a higher risk of cancer in a 5cm radius of the primary lesion. This risk can be up to 15-20
28
How may patients present at stage I/II of oral cancer?
1/3 of patients.
29
What is the cure rate for stage I oral cancer?
80%
30
What is the cure rate for stage II oral cancer?
65%
31
If oral cancer progresses beyond stage II, what is the 5 year survival and cure rate?
<50% survival, <30% cure
32
What are the typical treatments for oral cancer?
Surgery Radiotherapy Chemotherapy Immunotherapy
33
How would you identify lip cancer?
Non-healing ulcer or swelling
34
What are the two main risk factors for developing lip cancer?
Sunlight (UV) Smoking
35
How do lip cancers develop?
Slow growth Local invasion Rarely metastasise to nodes
36
What aspects should be considered about screening for oral cancers?
Benefits v harm Undetected lesions v false positives cost of screening v cost of disease cost of screening v harmful effects of disease
37
What screening tools are there for oral cancer?
HPV16 screening Toluidene blue VELscope Photodynamic diagnosis Clinical judgement
38
What are some drawbacks of using toluidine blue for oral cancer screening?
False positives in inflammatory lesions ~50% false negatives
39
What is the most effective and reliable oral cancer screening tool?
A trained GDP
40
What aspects of general practice are primary prevention for oral cancer?
Smoking cessation Alcohol reduction Healthy diet promotion
41
When should lesions be referred for review?
If it has not resolved within two weeks, and all potential causes have been managed.
42
What is the difference between a malignant and a benign lesion?
Benign tumours generally don't invade and spread, malignant cells are more likely to metastasize, or travel to other areas of the body. They also grow faster.
43
What is the WHO definition of Potentially malignant lesions?
- Altered tissue in which cancer is more likely to form
44
What is the WHO definition of potentially malignant condition?
- Generalised state with increased cancer risk
45
What are some potentially malignant conditions (systemic conditions)?
- Lichen planus (erosive or ulcerative on gingiva and tongue increased) - Oral submucous fibrosis - Iron deficiency - Tertiary syphilis
46
Why does a person with iron deficiency at higher risk of developing cancer?
- Iron deficiency leaves oral epithelium thinner - Oral epithelium vital part of proetcting against pathogens and carcinogens - When barrier is decreased - increased risk of infections of carcinogens
47
What are some potentially malignant lesions?
- Leukoplakia - Erythroplakia - Chornic hyperplastic candidiasis
48
What mucosa do most carcinoma in the UK arise from?
- Clinically normal mucosa
49
Where in the world does most cancer arise from potentially malignant lesions?
- High incidence arease - e.g. India
50
How many more time is leukoplakia likely to progress to cancer than clinically normal mucosa?
- 50 to 100 times
51
What is the most common type of white patch that can be scraped off?
- Acute pseudomembranous candidosis - aka thrush
52
What is leukoplakia?
- White patch which cannot be attributed to any other diagnosis
53
What is erythoplakia?
- Red patch that cannot be attributed to any other diagnosis
54
What are the predictors of malignancy in leukoplakia?
- Age (incidence increases with age) - Females more likely - Idiopathic (no risk factors ass with oral cancer more likely to become malignant) - Floor or mouth , tongue and gingivae have high risk - buccal mucosa has low risk - Non homogenous e.g. verrucous, ulcerated leuko-erythroplakia have higher risk than homogenous
55
What is it called when there is a white patch on the floor of mouth?
- Sublingual keratosis - Extremely high risk of developing into oral cancer
56
What is the gold standard for assessing malignant change in a lesion? What are we assessing?
- Histopathology - Dysplasia - Atrophy (thinner) - Candida infection (presence of candida hyphae - chronic hyperplastic candidiasis or aka candidal leukoplakia )
57
There is a new way being researched to assess malignant change by histopathology, what is it termed and what are we assessing?
- Biological markers - DNA content in leukoplakia showing hallmarks for future maligancy
58
What gene whether it has been mutated or other can be a strong indicator that the lesion is on its way to becoming malignant?
- p53
59
What is a risk factor of oropharyngeal cancer? What prognosis does this give?
- HPV - Presence of HPV gives better prognosis
60
What is dysplasia?
- Disordered maturation (growth) in a tissue
61
What is atypia?
- Changes in cells - Different to dysplasia
62
Describe why this picture is showing cellular atypia?
- Picture showing oral epithelium - Cells are more spaced out , not see well arranged in neat rows , looking a bit different to ones above it
63
What are the two categories of criteria for diagnosis of epithelial dysplasia from histopatholgy?
- Assess Architectural changes first (abnormal maturation and stratification) - Then assess Cytological changes (cellular atypia)
64
What is the WHO 2005 grading of epithelial dysplasia?
- Done via microscope ! - Hyperplasia - Mild - Moderate - Severe - Carcinoma-in-situ
65
What is basal hyperplasia in terms of histopathology?
- Increased basal cell numbers - Architecture has regular stratification and basal compartment is larger - No cellular atypia *arrow shows basal compartment being larger
66
What is mild dysplasia in regard to histopathology?
- Architectural changes in lower third - Cytological changes of mild atypia - Mild atypia such as pleomorphism, hyperchromatism
67
What is pleomorphism ?
- Variety of shapes and sizes - Can be from nucleus or cell or both together
68
What is hyperchromatism?
- Increased in DNA content therefore taking up more staining so appears darker purple on histopathologucal analysis
69
What are some factors that can contribute to mild dysplasia and what is likely to happen if these factors are removed?
- Trauma - Infection - Smoking - Removal of these factors likely to cease the mild dysplasia
70
What is moderate dysplasia in terms of histopathology?
- Architectural change extends into middle third of epithelium - Cytology : moderate atypia (plemorphism or hyperchromatism)
71
What is severe dysplasia in terms of histopathology?
- Architectural changes extend to upper third epithelium - Cytology: Severe atypia and numerous mitoses , abnormally high up in epithelium, loss of polarity, pleomorphism and hyperchromatism
72
Where does mitoses usually happen?
- At basal cell layer
73
What is carcinoma-in-situ?
- Theoretical concept - Malignant but not invasive (still contained within basement membrane of epithelium) - Abnormal architecture (full thickness of viable cell layers) - Pronounced cytological atypia with mitotic abnormalities frequent * Needs full removal if found in a pt
74
What is present in the underlying connective tissue if a pt has a malignancy?
- Inflammation - Shows pts has a immune response - If dysplasia present but no inflammation then pt is immunocompromised
75
Histopathology is the gold standard for malignancy prediction. What are some negatives hitsopathology?
- Invasive - Can't monitor tissue response to txt effectively as can't repeatedly take tissue samples to test response to txt - Not suitable for mass screening
76
What future technique are available for predicting malignancy?
- Salivary biomarkers - Next generation sequencing - Artificial intelligence
77
What are the two main factors of carcinogenesis?
- Genetics - Environmental damage
78
What is the very basic molecular basis of cancer?
- Damage to cells - Lead to altered gene expression - Lead to altered cell function
79
What are the 4 stages of carcinogenesis?
- Initiation where there is a change to gene such as carcinogen - Promotion of the cell via cell multiplication - Transformation of the cell via genetic change (mutation) into a malignant cell - Progression of the malignant cell via genetic change into malignant tumour
80
What are some examples of changes to genes that can occur?
- Change to chromosomes - Change to genes - Epigenetic changes
81
Give examples of changes to chromosomes
- Aneuploidy (extra or missing chromosome) - Translocations (rearrangement of chromosome) - Amplification
82
Give examples of changes to genes that can occur
- Mutations - Deletions - Amplifications
83
Give examples of epigenetic changes
- Chemical changes in DNA like methylation and modification of histone that package DNA
84
What types of HPV have oncological ability?
HPV 16 and HPV 18
85
Give the oral cancer genetic broad overview
- Oncogenes which produce normal growth factors - Tumour suppressor genes which suppress the growth of cells - growth of cells in body is in equilibrium between oncogenes and tumour supressor genes - Most active tumour suppresor gene is Tp53 either mutated or inactivated (in about 50-80% of head and neck cancer pt) - Genes that regulate apoptosis (cell death) if not done then cell continues lifespan - Genes involved in DNA repair - MiRNA (can play a role in neoplastic transformation) - chemo targets these
86
What is Knudson's two-hit hypothesis of carcinogenesis?
- Need both Tp53 tumour suppressor genes on the chromosome (pair) mutated or inactivated in order for carcinogenesis to occur
87
Do you need both of the oncogenes on a chromsome to be mutated or inactivated for malignant progression to occur?
- No oncogenes only need one to be mutated or inactivated for malignancy to occur - Tumour suppressor Tp53 requires both!
88
What are the 6 hallmarks of cancer? *KNOW
- Evading apoptosis - Self sufficiency in growth signals - Insensitivity to anti-growth signals - Tissue invasion and metastasis - Limitless replicative potential - Sustained angiogenesis
89
What is the filed change theory (field cancerisation)?
- If the area that the cancer was present has been removed this does not reduced the risk of oral cancer devloping in another area - there is genetic instability increasing the poss of devloping cancer - Clincally may appear normal and it is diff to estimate the extend of field - But multiple primaries of 15-20% - Can be synchronous or metachronous
90
What does synchronous mean?
- Primary malignancy that arise within 6 months of first maligancy
91
What does metachronous mean?
- Primary malignancy that arise more than 6 months apart
92
What are the important points that come back when oral cancer pathology report is performed?
- Diagnosis of squamous cell carcinoma - Differentiation and grading - Pattern of invasive front related to nodal spread - Local extension of disease
93
This image shows a cohesive front of dysplasia. What is meant by the term cohesive front?
- Cells advancing at the same rate and same time (sim to a wave)
94
What is meant by the term non-cohesive front?
- Cells advancing in clumps or strains at different rates - Positive correlation with lymph node involvement
95
How is the spread of oral cancer described?
1. Local extension of disease - Varies according to site i.e. mucosal extension, muscle (tongue), bone or nerve 2. Lymphatic spread 3. Haematogenous spread
96
How can tumour spread into bone?
- If pt is edentulous then via gaps in the cortex - If pt is dentate via periodontal ligament - bone destruction and increased mobility
97
What is meant by the term perineural spread?
- Involving small nerved at advancing edge predicts nodal spread - Extensive spread related to IAN may give recurrence
98
What are 3 ways lymphatic spread of oral cancer can occur?
- Via embolism - Via permeation - Via tumour involved node with extracapsular spread Require sentinal node biopsy
99
What is the clinical staging of oral cancer?
TNM
100
What are some rare types of OSCC?
- Verrucous carcinoma - Basaloid squamous (common in HPV) - Spindle cell (aggresive)

FINALS - Oral Medicine (13 decks)

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