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Oral Diseases and Microbiology > Histology > Flashcards

Histology Flashcards

1
Q

What type of epithelium is the palate?

A

Keratinised

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2
Q

What type of epithelium is the cheek?

A

Non-keratinised

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3
Q

What is acanthosis?

A

Hyperplasia of stratum spinosum

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4
Q

What are elongated rete ridges?

A

Hyperplasia of basal cells

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5
Q

What is keratosis in a non-keratinised site?

A

Parakeratosis

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6
Q

What is atrophy?

A

Reduction in viable layers

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7
Q

What is erosion?

A

Partial thickness loss

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8
Q

What is ulceration?

A

Full thickness loss with fibrin on surface

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9
Q

What is dysplasia?

A

Disordered maturation (growth) in a tissue
Atypia- changes in cells
Changes in appearance of cells, function, arrangement to other cells

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10
Q

What is an epulide?

A

Soft tissue swelling on the gingiva only
Reaction to chronic inflammation/chronic trauma
Can reoccur after removal if stimulus persists

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11
Q

What is a fibrous overgrowth?

A

Localised gingival hyperplasia
Can be:
–fibrous epulis
–vascular epulis (pyogenic granuloma)

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12
Q

What causes giant cell lesions?

A

Unphagocytosable materials
–local chronic irritation
–infective agents e.g. TB bacillus
–hormonal stimulation of cells- osteoclasts
Autoimmune- Sarcoidosis

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13
Q

What drugs can induce fibrous overgrowths?

A

Anti-hypertensives
–calcium channel blockers
Anti-epileptics
–phenytoin
Immunosuppressants
–cyclosporin

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14
Q

What is a potentially malignant condition?

A

Generalised state with increased cancer risk

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15
Q

What are some potentially malignant conditions related to the oral cavity?

A

Lichen planus
Oral submucous fibrosis
Iron deficiency
Tertiary syphilis

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16
Q

What is chronic hyperplastic candidosis?

A

Appears at the commissures of the lips
Dysplasia may be present
Common in smokers

17
Q

What is the pathology of chronic hyperplastic candidosis?

A

Special stain needed to demonstrate candida albicans hyphae clearly
PAS (periodic schiff stain)

18
Q

What is the treatment for chronic hyperplastic candidosis?

A

Systemic antifungals (fluconazole- 1xdaily for 14 days
Biopsy
Stopping smoking
Observe

19
Q

How many more x likely is leukoplakia to form cancer than clinically normal mucosa?

A

50 to 100 times

20
Q

What are the predictors of malignancy in leukoplakia?

A

Age
Gender
Idiopathic
Site
–buccal mucosa- low risk
–floor of mouth, tongue- high risk
Clinical appearance
–homogenous
–non-homogenous; verrucous, ulcerated

21
Q

What type of leukoplakia has the highest malignant transformation?

A

Proliferative verrucous leukoplakia

22
Q

What are the molecular markers in oral epithelial dysplasia?

A

Signalling pathways- EGFR
Cell cycle- K/67, p53, pRB
Immortalisation- telomerase
Apoptosis- p53, p21
Angiogenesis- VEGF
COX-1 & 2 enzymes
Proliferation and differentiation markers
Viruses- HPV+ and HPV-

23
Q

What is the epithelium of basal hyperplasia?

A

Increased basal cell numbers
Architecture
–regular stratification
–basal compartment is larger
No cellular atypia

24
Q

What is carcinoma-in-situ?

A

Theoretic concept
Malignant but not invasive
Abnormal architecture
–full thickness (or almost full) of viable cell layers
Pronounced cytological atypia
–mitotic abnormalities frequent

25
Q

What are the 2 main factors of carcinogenesis?

A

Genetic
Environmental (carcinogens)

26
Q

What is the molecular basis of cancer?

A

Damage
Altered gene expression
Altered cell function

27
Q

What is involved in oral cancer genetics?

A

Oncogenes- have normal roles within the cells, differing oncogenes activated
Tumour suppressor genes- suppress the growth of cells
P53 mutation or inactivation
Genes that regulate apoptosis
Genes involved in DNA repair
Viral component- HPB

28
Q

What can changes to genes include?

A

Changes to chromosomes (translocations, amplifications)
Genes (mutations, deletion, amplifications)
Epigenetic changes (chemical changes in DNA)

29
Q

What are the hallmarks of cancer?

A

Self-sufficiency in growth signals
Insensitivity to anti-growth signals
Evading apoptosis
Sustained angiogenesis
Tissue invasion & metastasis
Limitless replicative potential

30
Q

How does oral cancer spread?

A

Local extension of disease
–varies according to site
–mucosal extension
–muscle (tongue etc)
–bone
–nerve
Lymphatic spread
Haematogenous spread

31
Q

What is perineural spread?

A

Perineural spread involves small nerves at advancing edges which predicts nodal spread
Extensive spread related to inferior alveolar nerve may give recurrence

Oral Diseases and Microbiology (12 decks)

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