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Oral Medicine > Dysplasia > Flashcards

Dysplasia Flashcards

1
Q

What are the high risk sites for oral cancer?

A

FOM
Lateral border of tongue
Retromolar region
Soft and hard palate
Gingivae
Buccal mucosa

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2
Q

What are the risk factors for oral cancer and oropharyngeal cancer?

A

Smoking, betel quid chewing
- Increases with frequency, duration and quantity of tobacco used.
Alcohol- frequency more important than duration
UV exposure
Poor diet
Low socioeconomic status

Oropharyngeal cancer- HPV-16
- Sexual activity- six or more lifetime partners
- Four or more oral sex partners
- Early age of sexual debut

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3
Q

What are the chances of a white lesion turning into cancer?

A

Varied reports- most under 4%.

2.5% in 10 years, 4% in 20 years.

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4
Q

What type of mucosa do most oral carcinomas develop from?

A

Normal mucosa- not necessarily from what or red lesions.

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5
Q

Why is there a higher risk of malignant transformation of red lesions than white?

A

Red lesions suggest a change in vascular supply- i.e. increased vascular proliferation.

This process occurs in cancer.

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6
Q

What is dysplasia?

A

Disordered maturation in a tissue.

Can only be detected by means of a microscope- not a clinical diagnosis.

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7
Q

What is cellular atypia?

A

Describes changes in cells.

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8
Q

What is meant by the term potentially malignant lesion?

A

Altered tissue in which cancer is more likely to form.

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9
Q

Give examples of potentially malignant lesions.

A

Chronic hyperplastic candidosis

Proliferative verrucous leukoplakia

Erythroplakia

Leukoplakia

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10
Q

What is Chronic Hyperplastic Candidosis?

A

Persistent red/white speckled lesion caused by Candida albicans.

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11
Q

Where is chronic hyperplastic candidosis usually found?

A

Commissures of the mouth and sometimes the tongue.

Presents as a mixed red and white lesion, triangle shaped in the commissures of the mouth going posteriorly onto the buccal mucosa.

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12
Q

What cohort of patients usually have chronic hyperplasticity candidosis?

A

Smokers
Iron and folate deficiencies
Immune cell-mediated depletion

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13
Q

What does chronic hyperplastic candidosis look like clinically?

A

Found in the anterior commissures of the mouth

Discrete raised lesions that vary from small, palpable, translucent, whitish areas to large, dense, opaque plaques, hard and rough to the touch (plaque- like lesions)

Non-homogeneous

Speckled

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14
Q

If you suspect chronic hyperplastic candidosis, what would you do?

A

Refer for incisional biopsy of the lesion for histological analysis and periodic acid shiff stain.

Need to determine whether there is dysplasia present (histology) and also if there is candida species present (PAS).

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15
Q

What does chronic hyperplasticity candidosis look histologically?

A

Parakeratosis

Acanthosis

Inflammatory cells within the lamina propria- macrophages, lymphocytes and plasma cells.

Intra-epithelial invasion of immune cells

Margination and emigration of polymorphs from blood vessels into the tissue.

Hyperplastic epithelium

Mitotic figures higher up the epithelium than what is expected- usually only in the basal cell membrane.

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16
Q

What would the PAS show in chronic hyperplasticity candidosis?

A

Candida should stain pink- lots of glycogen in the cell walls of candida.

17
Q

According to the literature, what is the risk of malignant transformation of chronic hyperplastic candidosis?

A

9-40%

18
Q

What treatment should be done for chronic hyperplastic candidosis?

A

Smoking cessation and alcohol advice- educate the patient about why these are risks actors.

Biopsy and if it is mild dysplasia or higher- excise the whole lesion.

Systemic Fluconazole- 50mg one capsule a day for 14 days.

Ensure review regularly.

19
Q

What factors influence the prognosis of chronic hyperplastic candidosis?

A

Risk factors, such as tobacco and alcohol use

Whether the lesion is speckled (more dangerous) or
homogeneous

The presence (more dangerous) and degree of epithelial
dysplasia

The management adopted.

20
Q

How likely is a leukoplakia to turn to a malignancy?

A

50 to 100 times more than normal mucosa.

21
Q

What factors make it more likely for a leukoplakia to develop into a malignancy?

A

Older age

Site- FOM or lateral border of tongue are high risk sites

Non-homogenous- verrucous, ulcerated, leuko-erythroplakia.

22
Q

What is the gold standard for determining whether a leukoplakia is likely to become malignant?

A

Biopsy and histopathological analysis.

Look for
- Dysplasia
- Atrophy of the epithelium
- Candida infection

23
Q

What molecular markers might be used to determine oral epithelial dysplasia?

A

Signalling pathways- EGFR
Cell cycle- p53, pRB
Immortalisation- Telomerase
Angiogenesis- VEGF
COX1 and 2
HPV +ve

24
Q

What classification is used to grade dysplasia?

A

WHO classification 2005

Basal Hyperplasia
Mild
Moderate
Severe
Carcinoma in situ

25
Q

What is the criteria for diagnosis of dysplasia?

A

Architectural changes - abnormal maturation and stratification

Cytological abnormalities- cellular atypia

26
Q

Describe basal hyperplasia?

A

Increased basal cell numbers

Architecture- regular stratification, basal compartment is larger.

No cellular atypia

27
Q

What is mild dysplasia?

A

Architectural changes in the lower third

Mild atypia- pleomorphism, hyperchromatism, basal cell hyperplasia
Mitotic figures higher up than in the basal cell membrane.

28
Q

What is moderate dysplasia?

A

Architectural changes seen into the middle third

Moderate atypia- pleomorphism, hyperchromatism

29
Q

What is a severe dysplasia?

A

Architectural changes extend into upper Thord

Severe atypia- pleomprhism, hyperchromatism, loss of polarity of nucleus, numerous mitosis abnormally high.

30
Q

What is carcinoma in situ?

A

Abnormal architecture in full thickness of the epithelium.

Pronounced cytological atypia- mitosis abnormalities frequent.

Cytologically malignant but not invading.

Clinically may appear red and ulcerated- epithelium is thin.

31
Q

Describe the grading system of low, high and carcinoma in situ?

A

Low grade
- architectural change into lower third
- Cytological atypia or dysplasia may not be prominent
- Considerable amount of keratin formation- parakeratosis
- evidence of stratification
- Well formed basal cell layer

High
- Little resemblance to a normal squamous epithelium
- architectural change in the upper third
- considerable atypia
- invade in a cohesive pattern with fine cords, small islands and single cells infiltrating widely through the CT
- Mitotic figures are prominent.

32
Q

What cytological factors would suggest dysplasia?

A

Abnormal variation in cell size, cell shape, nuclear size, nuclear shape, nuclear hyperchromatism, atypical mitosis figures, increased/altered nuclear-cytoplasmic ratio.

33
Q

What architectural features would suggest dysplasia?

A

Irregular epithelial stratification

Loss/disturbed of polarity of basal cells

Drop-shaped rete pegs

Increased and abnormal mitoses

Abnormal keratinisation

Keratin pearls within rete pegs

34
Q

What are histological prognostic factors?

A

Invasion of vessels- associated with metastasis- poorer prognosis.

Perineural invasion

Depth of invasion of tissue

Pattern of invasion

35
Q

What oral cancer screening tools are available at the moment?

A

Vital staining- Toluidine blue, stains particular markers of the cel blue- not specific.

Oral cytology

Optical imaging- Velscope

HPV16 screening

Salivary biomarkers- research for the future.

36
Q

What is the molecular basis of cancer?

A

Altered gene expression, leads to altered cell function.

37
Q

What are the 6 factors that make up the hallmarks of cancer?

A

Self-sufficient growth signals

Insensitivity to anti-growth signals

Tissue invasion and metastasis

Limitless replicative potential

Sustained angiogenesis

Evading apoptosis

38
Q

State some of the OSCC subtypes.

A

Basaloid squamous

Spindle cell

Verrucous carcinoma

Oral Medicine (15 decks)

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