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

Potentially Malignant Disorders and Oral Cancer Flashcards

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?

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?

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
Q

What are the features of carcinoma in situ? (theoretical concept)

A

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
Q

What are the issues with histopathology confirmation of malignancy?

A

Invasive

Cannot monitor tissue response to treatment effectively

Not suitable for mass screening

27
Q

Which techniques may be used to monitor dysplastic changes in oral cavity in the future? (and recurrence/treatment effectiveness)

A

Salivary biomarkers

Next gen sequencing

AI

28
Q

What are the 2 main factors in carcinogenesis?

A

Genetic component

Environmental component (carcinogens)

29
Q

What happens to cells as a result of genes becoming mutated?

A

 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
Q

What are the stages in carcinogenesis?

A

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
Q

Which changes can occur in chromosomes that may lead to malignancy?

A

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
Q

Which changes can occur in genes that may lead to malignancy?

A

Mutations

Deletions

Amplifications- over-expressed factors

33
Q

Which epigenetic changes can occur that could lead to malignancy?

A

methylation of DNA (silences gene)

Histone modification (cannot regulate genes in normal way)

34
Q

What is an oncogene?

A

Gene responsible for producing normal growth factors

35
Q

What are tumour suppressor genes?

A

Genes that prevent growth of cells

-> Tp53 is most important- often becomes deleted, mutated or inactivated in cancer

36
Q

What are the oncogenic types of HPV and what do they produce?

A

HPV 16/18
-> produce E6 which degrades p53 (nothing to stop mutated cells dividing)

37
Q

What is the Knudsons 2 hit hypothesis?

A

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
Q

Which genes are commonly affected in oral cancer?

A

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
Q

What are the hallmarks of cancer and the type of drug used to combat it?

A

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
Q

Hallmarks and drugs continued:

A

Genome instability and mutation= PARP inhibitors

Resisting cell death= Proaptotic BH3 mimetic

Deregulating cellular Energetics= Aerobic glycolysis inhibitors

41
Q

What is the significance of polymorphic microbiomes against oral cancer?

A

The micro-organisms within the oral cavity may have protective effect against oral cancer

42
Q

What does the field change theory dictate?

A

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
Q

What are synchronous tumours?

A

New tumour that develops within 6 months of the primary tumour

44
Q

What are metachronous tumours?

A

New tumour that develops within a few years of primary tumour

45
Q

How is oral squamous cell carcinoma diagnosed? (most common in oral cavity)

A

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
Q

What are the features of a cohesive front in oral squamous cell carcinoma?

A

All cells advance at same rate (like a wave)

-> less likely to spread to LNs

47
Q

Where does oral cancer tend to spread to?

A

1.Local extension of disease (varies according to site)
-> mucosal extension
-> muscle (tongue etc)
-> bone
-> nerve
2. Lymphatic spread
3. Haematogenous spread

48
Q

What are the mechanisms in which oral cancer spreads to bone?

A

 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
Q

What part of nerves can tumours spread along? What is the significance of this?

A

Myelin sheath (of small nerves at advancing edge)
-> correlates to LN spread
-> difficult to erradicate
-> indicator that recurrence is likely

50
Q

How does spread of cancer to LNs occur?

A

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
Q

What is a sentinel node biopsy?

A

Principle draining LN of the malignancy is identified and taken out and studied
-> helps identify micro-metastases (clumps of malignant cells)

52
Q

How are tumours staged clinically?

A

 T- width, size
 N- LN involvement
 M- Metastases (distant)

53
Q

What does metastases by blood in carcinoma indicate?

A

Late stage disease

-> can spread to lungs and spine

54
Q

How does haematogenous spread of cancer occur?

A

Formation of malignant emboli which can be transported in blood

Growth of tumour in vein itself

55
Q

What are some examples of rarer forms of oral squamous cell carcinoma?

A

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
Q

TMN system:

A

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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