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BDS4 Oral Medicine > Potentially Malignant Disorders and Oral Cancer > Flashcards

Potentially Malignant Disorders and Oral Cancer Flashcards

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1
Q

What does the term potentially malignant disorders include?

A

Potentially malignant lesions

Potentially malignant conditions

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2
Q

What is a potentially malignant lesion?

A

Altered tissue in which cancer is more likely to form

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3
Q

What is a potentially malignant condition?

A

Generalised state/condition associated with increased cancer risk

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4
Q

What are examples of systemic conditions which are considered potentially malignant?

A

lichen planus- erosive/ulcerative variants (esp on tongue or gingiva)

Oral Submucous fibrosis- associated with chewing of betel nut

Iron deficiency

Tertiary syphilis

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5
Q

What occurs in Oral Submucous Fibrosis?

A

 Abnormal collagen deposits in connective tissue of submucosa
 Makes expansion and movement different
 Muscles undergo degradation
 Limited mouth opening

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6
Q

What makes iron deficiency a potentially malignant condition?

A

Associated with thinning of mucosa- easier passage of pathogens and carcinogens into tissue

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7
Q

How can tertiary syphillis present intra-orally?

A

As a mass of granulation tissue on tongue (can also get leukoplakia like lesions)

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8
Q

What is leukoplakia?

A

Clinical diagnosis:
 White patch- can’t determine underlying cause (can’t be scraped off)

-> Higher risk of malignant transformation than normal mucosa (depends on other patient factors- habits etc)

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9
Q

What is a white patch that can be wiped off likely to be?

A

Acute pseudomembranous candidiasis (thrush)

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10
Q

What are the clinical predictors for malignant change in leukoplakia lesions?

A

Older age

Female sex

Idiopathic cause- lack of risk factors, unexplainable lesion

Site- floor of mouth and tongue are high risk

Non-homegenous lesions

Verroucous/Ulcerated erythroleukoplakia

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11
Q

What are histopathology assessment of potentially malignant lesions useful for showing us?

A

Dysplasia

Atrophy- seen in erythroplakia

Candida infection

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12
Q

Which type of candida infection is associated with malignancy?

A

Chronic hyperplastic Candidosis (candida leukoplakia)
 Purely white or mixed red and white lesion
 Associated with smoking

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13
Q

Why may it be useful to look at the DNA content of leukoplakia lesions when assessing malignant potential?

A

As increased copies of genes present within chromosome can be a hallmark that the cell is carrying signs of malignant change

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14
Q

Which molecular markers are commonly found in oral epithelial dysplasia?

A

Enzymes- cox1/2

Viruses

Growth factors- VEGF

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15
Q

What is the purpose of p53 protein?

A

Helps stop cell division when there is genetic damage present

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16
Q

What is the different about the gene that codes for p53 in malignancy?

A

It is often missing, inactive or mutated

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17
Q

What is unusual about HPV+ pro-pharyngeal cancer?

A

Better prognosis than HPV-

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18
Q

What is dysplasia?

A

Disordered growth or maturation of a tissue

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19
Q

What is cellular atypia?

A

Changes in cells:
 Spaces appearing- separation
 Poor arrangement- not neat
 Strange appearance
-> darker (takes different amount of stain- hyperchromatism)
-> Neomorphism (variety of shapes and sizes in nucleus or cells)

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20
Q

What are the grades of epithelial dysplasia? (done using microscope)

A

hyperplasia

mild

moderate

severe

carcinoma-in-situ

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21
Q

What are the features of basal hyperplasia?

A

Increased basal cell numbers- act as stem cells in basal compartment

Architecture:
regular stratification
basal compartment is larger

No cellular atypia

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22
Q

What are the features of mild dysplasia?

A

 mild atypia- not all cells are showing signs
 In lower third only
 Reactive- infection, trauma, smoking (remove cause- this will likely regress)

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23
Q

What are the features of moderate dysplasia?

Study These Flashcards
A

Dysplastic change extends into middle third

Moderate atypia- spacing present, pleomorphism, hyperchromatism

More round and bulbous rete ridges

24
Q

What are features of severe dysplasia?

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A

 Extends into upper third

 Severe atypia- Widespread dark nuclei (hyperchromatism), loss of polarity

 Multiple mitoses- cells undergoing division closer to surface (should occur at basal layer only)

25
What are the features of carcinoma in situ? (theoretical concept)
Malignant but not invasive- confined to epithelium (contained by BM- no spread to connective tissue) Affects full thickness of epithelium Pronounced atypia -> wide rete pegs -> Widespread mitotic abnormalities Inflammation of underlying connective tissue (indicative of immune reponse)
26
What are the issues with histopathology confirmation of malignancy?
Invasive Cannot monitor tissue response to treatment effectively Not suitable for mass screening
27
Which techniques may be used to monitor dysplastic changes in oral cavity in the future? (and recurrence/treatment effectiveness)
Salivary biomarkers Next gen sequencing AI
28
What are the 2 main factors in carcinogenesis?
Genetic component Environmental component (carcinogens)
29
What happens to cells as a result of genes becoming mutated?
 Every gene produces a protein which carries out a function  Mutation causes gene product to be inactivated or over/under expressed  Gene expression is altered- target for protein is changed  Alteration in function of the cell
30
What are the stages in carcinogenesis?
Initiation- mutation occurs in gene (cell can divide carrying that mutation- which may not repair) Promotion- secondary mutation occurs in genes that code for reparation of DNA -> this may become malignant now Transformation- cell then cannot repair DNA damage (genome can become unstable) Progression- cell becomes malignant and divides/multiplies eventually forming tumour
31
Which changes can occur in chromosomes that may lead to malignancy?
Aneuploidy- abnormal number Translocations- part of one chromosome breaks off and attaches to another (can cause unwanted activation of other chromosomes) -> leukaemia Amplifications- extra copies of genes
32
Which changes can occur in genes that may lead to malignancy?
Mutations Deletions Amplifications- over-expressed factors
33
Which epigenetic changes can occur that could lead to malignancy?
methylation of DNA (silences gene) Histone modification (cannot regulate genes in normal way)
34
What is an oncogene?
Gene responsible for producing normal growth factors
35
What are tumour suppressor genes?
Genes that prevent growth of cells -> Tp53 is most important- often becomes deleted, mutated or inactivated in cancer
36
What are the oncogenic types of HPV and what do they produce?
HPV 16/18 -> produce E6 which degrades p53 (nothing to stop mutated cells dividing)
37
What is the Knudsons 2 hit hypothesis?
Within pairs of chromosomes  There are a pair of tumour suppressor genes (one in each chromosome)- both of these must be mutated or lost to cause malignancy  If oncogenes becomes mutated it only requires one for malignancy to occur
38
Which genes are commonly affected in oral cancer?
Oncogenes Tumour supressor genes Genes involved in apoptosis (natural cell death) -> without this cells would continue to divide DNA repair genes MiRNA- strands of RNA associated with neoplastic change
39
What are the hallmarks of cancer and the type of drug used to combat it?
Sustaining proliferative signalling= EGFR inhibitors Evading growth suppressors= Cyclin-dependent kinase inhibitor Avoiding immune destruction= Immune activating anti-CTLA4 mAb Enabling replicative immortality= Telomerase inhibitors Tumour promoting inflammation= selective anti-inflammatories Activating invasion and metastasis= Inhibitors of HGF/c-met Inducing angiogenesis= Inhibitors of VEGF signalling
40
Hallmarks and drugs continued:
Genome instability and mutation= PARP inhibitors Resisting cell death= Proaptotic BH3 mimetic Deregulating cellular Energetics= Aerobic glycolysis inhibitors
41
What is the significance of polymorphic microbiomes against oral cancer?
The micro-organisms within the oral cavity may have protective effect against oral cancer
42
What does the field change theory dictate?
That areas around malignancy are more likely to become malignant (as the whole area could be subjected to the changes which cancer site) -> if oral cancer- higher risk of pharynx, larynx, respiratory tract malignancy
43
What are synchronous tumours?
New tumour that develops within 6 months of the primary tumour
44
What are metachronous tumours?
New tumour that develops within a few years of primary tumour
45
How is oral squamous cell carcinoma diagnosed? (most common in oral cavity)
Grade (based on differentiation seen on microscope)- well, moderate*, poorly, anaplastic Pattern of invasive front -> non-cohesive suggests LN spread Local extension of disease
46
What are the features of a cohesive front in oral squamous cell carcinoma?
All cells advance at same rate (like a wave) -> less likely to spread to LNs
47
Where does oral cancer tend to spread to?
1.Local extension of disease (varies according to site) -> mucosal extension -> muscle (tongue etc) -> bone -> nerve 2. Lymphatic spread 3. Haematogenous spread
48
What are the mechanisms in which oral cancer spreads to bone?
 Via gaps in cortex  Via PDL (in dentate patients ) -> presents as unexplained mobility in patients with good OH (requires investigation as tumour may be causing bone disruption)
49
What part of nerves can tumours spread along? What is the significance of this?
Myelin sheath (of small nerves at advancing edge) -> correlates to LN spread -> difficult to erradicate -> indicator that recurrence is likely
50
How does spread of cancer to LNs occur?
Permeation- cancerous cells grow within lymphatic vessels Embolism- parts of the malignancy area break off and travel within lymphatic vessels to node Extracapsular- malignant cells can grow outside the node and spread to surrounding area
51
What is a sentinel node biopsy?
Principle draining LN of the malignancy is identified and taken out and studied -> helps identify micro-metastases (clumps of malignant cells)
52
How are tumours staged clinically?
 T- width, size  N- LN involvement  M- Metastases (distant)
53
What does metastases by blood in carcinoma indicate?
Late stage disease -> can spread to lungs and spine
54
How does haematogenous spread of cancer occur?
Formation of malignant emboli which can be transported in blood Growth of tumour in vein itself
55
What are some examples of rarer forms of oral squamous cell carcinoma?
Verrucous (outward growing, thick, warty)  Slow progressing  Rarely metastasis  Better prognosis Basaloid (appear like basal cells)- associated with HPV Spindle cell (cells appear like fibroblasts)- aggressive
56
TMN system:
T – tumour: § Tx – no available info on primary tumour § To – no evidence of primary tumour § TIS – only carcinoma in situ on primary sites § T1 - <2cm § T2 – 2-4cm § T3 - >4cm § T4 - >4cm, involvement of antrum, pterygoid muscles, base of tongue or skin N – node: § Nx – cannot be assessed § N0 – no clinical positive nodes § N1 – single, ipsilateral <3cm § N2a – single, ipsilateral 3-6cm § N2b – multiple, ipsilateral <6cm § N3a – single/multiple, ipsilateral node, one more than 6cm § N3b – bilateral § N3c – contralateral M – metastasis: § Mx – not assessed § M0 – no evidence § M1 – distant metastasis present

BDS4 Oral Medicine (28 decks)

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