10. Oral Medicine

Question 1

Oral Epithelium Reactions

Define:

1. Keratosis
2. Acanthosis
3. Elongated rete ridges
4. Atrophy
5. Erosion
6. Ulceration
7. Oedema
8. Blister

Answer 1

1. Keratin formation in non-keratinised sites
2. Hyperplasia of stratum spinosum
3. Basal cell hyperplasia
4. Thinning of normal epithelium, reduction in viable layers
5. Partial thickness loss of epithelium
6. Full thickness loss of epithelium
7. Intracellular or intercellular (spongiosis) fluid accumulation and swelling
8. Localised accumulation of fluid (vesicle <0.5mm, bulla >0.5mm)

Question 2

White Lesions 1

1. 2 causes of chemical burns
2. 2 clinical features
3. Management
4. 8 differential diagnoses for white patches
5. 2 types of hereditary white patches
6. Clinical appearance of both
7. Management of both

Answer 2

1. Drug-induced (aspirin burns), oral candidiasis, ingestion of bleach/strong acid
2. Transient white patch, mucosal sloughing, superficial epithelial necrosis
3. Remove cause
4. Hereditary, frictional, smoking, LP, SLE, chronic hyper plastic candidosis, carcinoma, leukoplakia
5. White sponge naevus, fordyce spots/granules
6. White sponge naevus - asymptomatic, diffuse, soft unevening thickening of superficial epithelium, often on non-keratinised mucosa. Widespread oedema
   Fordyce spots/granules - visible inactive sebaceous glands. Small, raised white/pale/red spots/bumps (1-3mm diameter), usually on vermillion border, buccal mucosa, genitals
7. Reassurance and symptomatic relief

Question 3

White Lesions 2

1. Causes of frictional keratosis
2. Clinical appearance
3. 3 histological features
4. Management
5. Cause of smokers keratosis and commonly affected sites
6. Clinical appearance
7. 3 histological features
8. Management
9. Definition of leukoplakia
10. Histological appearance
11. 2 types of leukoplakia and appearance
12. Risk of malignant transformation

Answer 3

1. Response to chronic low grade trauma. Sharp cusps/restoration, ill-fitting denture, cheek biting
2. White patch surrounded by red inflammation, erosion/ulcer/blister surrounded by red halo, yellow fibrinous (or red raw) base
3. Epithelial (hyper)keratosis, variable dysplasia, minimal infiltrate
4. Remove source (adjust denture, trim cusp/restoration, provide splint) and review. If no signs of healing within 3 weeks, urgent biopsy
5. Low-grade burn and chemical irritation
6. Painless white keratitis layer with the presence of small red spots (blocked sebaceous glands)
7. Hyperkeratosis, variable dysplasia, minimal infiltrate
8. Smoking cessation
9. White patch which cannot be scraped/rubbed off or attributed to any other cause. Diagnosis of exclusion
10. Wide range - normal to carcinoma-in-situ. Keratosis, acanthuses, cellular atypic, infiltration of corneum by plasma cells
11. Hairy - bilateral white, non-removable corrugated lesions of tongue. Associated with HIV, EBV, lymphoma
    Panoral - entire oral mucosa appears to be undergoing hyper plastic field changes
12. 1-5%

Question 4

White/Red Lesions

1. Define erythroleukoplakia
2. How to manage erythroleukoplakia
3. Define erythroplakia
4. How to mangage erythroplakia

Answer 4

1. Mixed white and red patch
2. Urgent biopsy
3. Red patch which cannot be rubbed off or attributed to any other cause
4. Urgent biopsy

Question 5

Pigmented Lesions 1

1. 2 causes of exogenous pigmentation
2. 2 causes of endogenous pigmentation
3. 3 types of localised
4. 3 types of generalised
5. Clinical appearance of amalgam tattoo
6. Aetiology
7. 2 histopathological findings
8. Management
9. Macule appearance
10. Management
11. Melanocytic naevus appearance
12. Management
13. Syndrome associated with multiple naevi and 1 other feature

Answer 5

1. Amalgam, heavy metals
2. Melanin, haemosiderin
3. Amalgam tattoo, macule, naevi, KS, melanoma, pigmentary incontinence
4. Physiological, smoking, medications, adrenal insufficiency, ACTH-producing pathology, paraneoplastic phenomenon
5. Dense blue/black/grey area of mucosal pigmentation (near amalgam restoration)
6. Amalgam in tissue Brough to surface by macrophages
7. Multinucleate giant cells surrounded by amalgam fragments
8. Biopsy if concerned, or use previous radiographs. Reassure
9. Usually solitary, <1cm diameter, well-defined, flat border. Usually lower lip. Freckle-like
10. Diagnosis, biopsy if concerned, reassure
11. Melanocytic tumour containing naevus cells, known as a mole. Common on vermillion border and palate. Can be >1cm, no change in size or colour
12. Clinical or biopsy, reassure, review
13. Peutz-Jeghers. Benign hamartomatous polyps in GIT and multiple small peri-oral naevi

Question 6

Pigmented Lesions 2

1. What is Kaposi’s sarcoma linked to
2. Clinical appearance
3. 2 risk factors
4. 2 types
5. Diagnosis and management
6. Clinical appearance of malignant melanoma
7. Cause of IO melanoma
8. 4 causes of secondary melanosis
9. What drug can cause dry mouth
10. 2 drugs that can cause infections
11. 3 drugs that can cause lichenoid reactions
12. 3 drugs that can cause gingival hyperplasia
13. 3 drugs that can cause pigmentation
14. 1 drug that can cause characteristic ulceration

Answer 6

1. HHV-8 and HIV
2. Red/purple, can occur individually, in groups, widespread. Flat or raised, slow or fast progression
3. Immunosuppression, chronic lymphoedema
4. Endenic, classic, epidemic, immunosuppression therapy-related
5. Biopsy. Surgery, radio, chemo, biologics, HAART
6. Changes in mole size, shape, colour (very dark), itchy, skin breakdown, bleeding
7. Unknown (UV exposure on skin/lips)
8. Smoking, drug-related, inflammation, Addison’s disease/adrenal insufficiency
9. Iron supplements
10. Steroids, antifungals
11. ACE inhibitors, beta-blockers, diuretics, nifedipine, NSAIDs, anticonvulsants, omeprazole, tetracycline, oral hypoglycaemic, antimalarials
12. Phenytoin, cyclosporin-A, nifedipine
13. Antimalarials, chlorhexidie MW, OCP, cisplatin, phenothiazines, hydroxychloroquine
14. Nicorandil

Question 7

Vascular lesions

1. 2 types and define them
2. 2 types of one
3. Clinical appearance of both
4. Syndrome associated with vascular malformations
5. Define lymphangioma

Answer 7

1. Haemangioma - benign vascular tumour derived from blood vessel cell types. Strawberry mark (infantile). Developmental.
   Vascular malformation - BV or lymph vessel abnormality, can present at any time
   Both blanch on pressure
2. Cavernous, capillary
3. Cavernous - larger, blue/purple
   Capillary - smaller, red
4. Sturge-Weber - port wine stain that runs in distribution of CNV
5. Malformation of lymphatic system characterised by thin-walled cyst lesions. Commonly in <2yrs old.

Question 8

Lip and Tongue Abnormalities 1

1. Define geographic tongue and how common is it
2. Describe aetiology
3. Describe clinical appearance
4. Describe management
5. 3 histopathological features
6. 2 causes of glossitis
7. Clinical appearance
8. Management
9. Causes of coated tongue and management

Answer 8

1. Common, benign, inflammatory condition. 1-2% adults
2. Unknown
3. Rapid appearance and disappearance of atrophic (red) areas with a white demarcated border on the dorsal surfaces of the tongue with temporary loss of filiform papillae (depapillation). Variable daily appearance
4. Dietary advice (avoid hot, spicy foods, avoid SLS) and symptomatic relief (benztdamine)
5. Central lesion erosion, mild peripheral hyperplasia and hyperkeratosis, chronic inflammatory cells in underlying CT
6. Vitamin/nutritional deficiencies, haematological conditions
7. Beefy-tongue, loss of papilla, lobulated if severe, smooth red shiny dorsal surface
8. Symptomatic relief, correction of any underlying deficiency or condition
9. Build-up of normal cellular debris on dorsal. Dehydration, illness, poor diet. Cause-related therapy, removal with abrasive instrument

Question 9

Soft Tissue Swellings 1

1. Define epulis
2. 3 histological features
3. Definition of denture-induced hyperplasia
4. Aetiology
5. Clinical appearance
6. Management
7. 2 other types of fibrous overgrowths caused by dentures
8. Define pyogenic granuloma
9. What else can it be known as
10. Clinical appearance
11. Aetiology
12. Management
13. Define pregnancy epulis
14. Management

Answer 9

1. Any tumour-like enlargement situated on gingival or alveolar mucosa
2. Granulation tissue formation, chronic inflammatory cells, vascular lesion, metaplastic bone formation sometimes (reactive change), sometimes ulcerated epithelium
3. Fibrous hyperplasia of excess CT folds
4. Reaction to chronic trauma from ill-fitting denture. Common hyper plastic response to repeated trauma
5. Erythematous mucosa, keratosis, bleeding
6. Denture adjustments
7. Leaf fibroma, papillary hyperplasia of palate
8. Vascular lesion
9. Vascular epulis if beneath gingival margin
10. More common in younger people, red/purple, nodule, bleeds easily, sessile or pedunculated
11. Reaction to recurrent trauma or low-grade infection
12. Excision, debridement, OHI
13. Pyogenic granuloma in pregnant females
14. OHI, reassurance monitor

Question 10

Soft Tissue Swellings 2

1. Aetiology of fibre-epithelial polyp
2. Appearance
3. 3 histological features
4. Management
5. Other name for giant cell epulis
6. Distintive features/clinical appearance
7. Aetiology
8. 3 histological features
9. Management
10. 2 differential diagnoses
11. Other name for warts
12. Aetiology
13. Management

Answer 10

1. Response to low-grade recurrent trauma
2. Pink, red or white growth of varying sizes. Common on BM, lips, tongue, relatively avascular, keratotic
3. Thick fibrous core, few BVs and chronic inflammatory cells, keratinised stratified squamous epithelium
4. Excision, monitor, remove cause
5. Peripheral giant cell granuloma
6. Deep red gingival swelling, round, soft, bleed profusely, no fibrous tissue capsule
7. Chronic low-grade trauma (material cannot be phagocytosed)
8. Vascular lesion, multinuclear giant cells
9. Excision, removal of cause
10. Brown tumour, central giant cell granuloma, aneurysmal bone cyst, giant cell tumours
11. Squamous papillomata
12. HPV
13. Excision

Question 11

Hard Tissue Swellings 3

1. 4 types of developmental non-tumour hard tissue pathologies
2. 2 types of inflammatory
3. 2 types of metabolic
4. Appearance of tori
5. Management
6. Aetiology of OI
7. 4 associated features
8. What is osteomyelitis
9. 3 causes of bone necrosis
10. Pathophysiology of osteoporosis
11. IO consequence of hyperparathyroidism
12. Define Brown tumour
13. 3 histological features

Answer 11

1. Tori, OI, fibrous dysplasia, condensing osteitis, achondroplasia, osteopetrosis
2. Osteomyelitis, alveolar osteitis, bone necrosis
3. Osteoporosis, osteomalacia, hyperparathyroidism
4. Palatinus - midline of palate
   Mandibularis - bilateral, lingual premolar/molar area
5. No treatment, remove if symptomatic/obviously enlarging/interfering with denture construction
6. Type 1 collagen defect
7. Blue sclera, weak bones, multiple easy fractures, DI
8. Rare endogenous infection
9. Osteomyelitis, avascular necrosis (anti-resorptive, bisphosphonates, bone metastases, multiple myeloma, osteoporosis), irradiation (ORN)
10. Bone atrophy - resorption occurs more than formation leading to an endosteal net loss (quantitative deficiency)
11. Osteitis fibrosa cystica (Brown tumour)
12. Osteitis fibrosa cystica - giant cell lesion within bone (bone swelling). Regresses if hyperparathyroidism appropriate treated
13. Multinucleated giant cells, haemosiderin, cystic cavities

Question 12

Viral Infections 1

1. 4 common viruses
2. 8 types of HHV
3. HSV 2 types and description
4. Clinical features of primary HSV (and other name)
5. Management
6. 2 histological features
7. Pathogenesis of recurrent HSV
8. Common oral presentation
9. 4 causes
10. Disease progression
11. Management
12. Description of VZV
13. Clinical appearance of varicella
14. Clinical appearance of zoster
15. Management of VZV

Answer 12

1. HHV, coxsackie virus, measles, HPV
2. HSV 1, HSV II, VZV, EBV, CMV, HHV6, HHV7, HHV8
3. Type I (dominant orally), type II (genital infections usually)
4. Primary herpetic gingivostomatitis - widespread shallow vesicles (break down to ulcers), gingival erythema, fever, malaise, halitosis, enlarged tender lymph nodes
5. Self-limiting. Benzydamine, bed rest, analgesia, fluids
6. Ballooning degeneration of epithelial cells and intranuclear Lipshutz bodies
7. Reactivation of primary infection which is believed to lie dormant in dorsal root and trigeminal ganglia.
8. Herpes labialis, crop of blisters that crust over
9. Trauma, sunlight, stress, immunocompromise (illness)
10. Prodromal phase (burning/tingling), cold sore appearance
11. High dose acyclovir during periods of acute infection (cream during prodromal phase), LT low-dose acyclovir, fluids, analgesia
12. Varicella - primary infection
    Zoster - reactivation of latent virus from sensory ganglion
13. Centripetal rash, fully body cutaneous spots, itchy, prone to bleeding
14. Confined to distribution of nerve it remains dormant in. Unilateral lesion, never crossing midline, sometimes CN V. Painful vesicles, rupture to ulcers, crusting, scarring, pigmentation
15. Bed-rest, fluids, analgesia; acyclovir, topical steroids

Question 13

Viral Infections 2

1. What does EBV cause
2. Clinical appearance
3. Management
4. What does CMV cause
5. 2 diseases that Group A Coxackie causes
6. Clinical appearance of herpangina
7. Management
8. What virus causes HFM disease
9. Clinical appearance
10. Management
11. 2 types of HPV involved with OPSCC
12. How to prevent
13. Clinical appearance of measles
14. How to prevent
15. How does acyclovir work against HHV

Answer 13

1. Infectious mononucleosis (MONO)
2. Sore throat, generalised lymphadenopathy, fever, headaches, malaise, maculopapular rash
3. Bed rest, fluids, analgesia
4. Glandular fever
5. Herpangina, hand foot and mouth disease
6. Widespread small (pinhead) ulcers on uvula, palate and fauces, fever, sore throat, conjunctivitis
7. Self-limiting - bed rest, fluids, analgesia
8. A16 (or A5 or A10)
9. Papular, vesicular rash on hands and feet, oral vesicles which rupture into superficial painful ulcers (widespread, small pinhead - herpangina-like but with hands and feet too)
10. Self-limiting - bed rest, fluids, analgesia
11. Types 16, 18
12. Vaccination
13. Koplik’s spots, maculopapular rash behind ears, round to face and trunk
14. MMR vaccine
15. Blocks herpes DNA polymerase from fabricating more herpes vDNA. Inhibits herpes thymidine kinase, blocking growing chain of viral nucleic acids

Question 14

Bacterial Infections

1. Appearance of primary syphilis IO
2. Appearance of secondary syphilis IO
3. Appearance of tertiary syphilis IO

Answer 14

1. Chancre - painless ulcerated nodule at site of inoculation, cervical lymphadenopathy
2. Cutaneous rash, condylomata, sensitive sloughy mucosa, serpiginous ulceration, malaise, fever, weight loss
3. Gumma - necrotic granulomatous reaction, enlarges and ulcerates, multi system disorder

Question 15

Fungal Infections 1

1. How does oral candidosis occur
2. 5 types of candida species
3. 3 virulence factors
4. How to histo test for candida
5. 3 types of candidosis
6. Describe clinical appearance of acute pseudomembranous
7. Management
8. Clinical appearance of erythematous candidosis
9. Management
10. 3 causes
11. Other name for chronic hyper plastic candidosis
12. Clinical appearance
13. What is unique about this
14. How to diagnose
15. 3 histological features
16. Management

Answer 15

1. Altered regulation of oral microflora, some commensal organisms eradicated allow others to flourish, overgrow and become pathogenic
2. Auris, albicans, tropicalis, krusei, glabrata
3. Hyphae, adherence, extracellular enzymes
4. PAS (doesn’t show up (well) on H&E stain)
5. Acute pseudomembranous, chronic erythematous, chronic hyper plastic, chronic atrophic, chronic mucocutaneous
6. White plaques, lightly adherent, can be rubbed off, discomfort eating, burning sensation, bad taste
7. Antifungals, CHX MW
8. Atrophic mucosa, shiny red appearance
9. Treat cause, steroids, antifungals, CHX MW
10. Denture related, antibiotic stomatitis, surgery, IVDU, indwelling catheter
11. Candidal leukoplakia
12. White, nodular patch, often oral commissures and buccal mucosa and dorsal tongue. Unilateral or bilateral
13. Increased risk of malignant transformation
14. Biopsy (histo and micro)
15. Keratosis, epithelial hyperplasia, increased mitotic activity, polymorph cell accumulation
16. Antifungals, correct cause (smoking cessation, vitamin deficiency), surgical excision if dysplastic

Question 16

Fungal Infections 2

1. What type of candidosis is denture-induced stomatitis
2. Clinical appearance/features
3. Management
4. Classification
5. Example of chronic atrophic candidosis
6. Clinical appearance
7. 2 causes
8. 3 histological features
9. Management
10. Type of pathogens involved in angular cheilitis
11. Clinical appearance
12. 3 causes
13. Diagnosis
14. Management
15. Describe how antifungals work

Answer 16

1. Chronic erythematous candidosis
2. Widespread erythema on mucosal surface underlying fitting denture surface. Red mucosa, burning sensation, bad taste; often asymptomatic
3. Remove candida from denture base (antiseptic, denture hygiene, nystatin gel before fitting), antifungals, CHX MW
4. Type I - pinpoint/localised inflammation (hyperaemia)
   Type II - diffuse inflammation/erythema
   Type III - granular inflammation/erythema (papillary hyperplasia)
5. Median rhomboid glossitis
6. Flat, depressed, midline of dorsal, posterior 2/3 of tongue, nodular red/pink, depapillation
7. Smoking, inhaled steroids
8. Epithelial atrophy, broad parallel-sided rete process hyperplasia, infiltrate, broad band of dense scarred fibrous tissue
9. Often none, symptomatic relief
10. S. aureus, C. albicans
11. Red, cracked skin at angles of mouth, gold crust
12. Trauma, inadequate denture VD, vitamin deficiencies (iron, B12)
13. Culture swab, bloods (FBC)
14. Miconazole cream/gel (often with hydrocortisone)
15. Polyenes - nystatin - fungicidal. Directly target ergosterol in cell wall, causing perforation and leakage of intracellular contents
    Azoles - fluconazole - fungistatic. Target ergosterol in cell wall by interrupting activity of enzyme involved in its production, 14a demethylase. risk of resistance (krusei and glabrata are naturally resistant)

Question 17

Oral Ulcerations 1

1. 5 causes of OU
2. Appearance of traumatic ulceration
3. Management
4. Aetiology of RAS
5. 3 types
6. How common is minor RAS
7. Clinical appearance
8. 3 exacerbating factors
9. Management
10. How common is major RAS
11. Clinical appearance
12. 3 systemic conditions major RAS is associated with
13. Management
14. How common is herpetiform RAS
15. Clinical appearance
16. Management
17. What is the Behcet’s triad
18. 3 other clinical features
19. Management

Answer 17

1. Trauma, cancer, immunological (RAS, LP, SLE), infections (HHV, bacterial, fungal), Behcet’s disease, VB diseases (pemphigus, pemphigoid), drugs (nicorandil)
2. Normal/white margin surrounding red/yellow CT base
3. Remove cause, biopsy if no healing after 2-3 weeks
4. Unknown - immunological, associated with T-cell mediated basal cell destruction. Links with nutritional deficiency, immunosuppression, familial traits
5. Minor, major, herpetiform
6. Up to 25% of population
7. Small (<5/10mm diameter), non-keratinised mucosa, small cluster. Red halo surrounding yellow base. 1-2 weeks, heal without scarring. Recur
8. Smoking, stress, local trauma, menstruation, SLS, NSAIDs, bisphosphonates, allergies
9. Prevent infection, symptomatic relief
10. 10% of all RAS
11. > 10mm diameter, more severe, more frequent, often multiple, keratinised or non-keratinised mucosa. 5-10 weeks, scar, tissue destruction
12. GI disorders, haem disorders, AIDS
13. Prevent infection, symptomatic relief, systemic steroids if required
14. 5% of all RAS
15. Non-keratinised mucosa, large crop (100) of small (1-2mm diameter) painful ulcers. 2 weeks, do not scar. May merge into larger areas of ulceration. Usually FoM, lateral/tip of tongue, recur
16. Prevent infection, symptomatic relief, systemic steroids if required
17. Minor RAS, genital ulcers, uveitis
18. Arthritis, skin pustules, neuro disease, GI disease, vasculitis
19. MDT (derm, OM, rheum, ophth, etc.). Symptomatic relief, sometimes anti-TNF therapies

Question 18

Immunological Diseases 1

1. Define the 4 types of hypersensitivity reactions
2. Name 3 local immunological oral diseases
3. Name 4 systemic immunological diseases with oral presentations
4. 2 methods of diagnosing immune-mediated diseases
5. What are 2 features of vesiculobullous diseases
6. Name 4
7. What is dermatitis herpetiformis associated with
8. Management
9. What is ABH
10. Common site affected
11. Management
12. What are the 4 types of EB
13. What is desquamative gingivitis
14. 3 causes
15. Management
16. What type of hypersensitivty reaction is erythema multiforme
17. Aetiology
18. Clinical presentation
19. Management
20. Syndrome associated with severe erythema multiforme
21. Management

Answer 18

1. Type I - IgE mediated
   Type II - cytotoxic
   Type III - immune comple
   Type IV - cell-mediated
2. RAS, lichen planus, OFG, lupus erythematosus
3. Erythema multiforme, Sjogren’s, SLE, systemic sclerosis, pemphigus, pemphigoid
4. Biopsy for histology (H&E) and direct immunofluorescence
5. Vesicles (<5-10mm diameter) and bullae (>5-10mm diameter)
6. Pemphigoid, pemphigus, angina bullosa haemorrhagica, dermatitis herpetiformis, linear IgA disease, epidermolysis bullosa
7. Gluten sensitivity
8. GF diet
9. Formation of blood blisters in the absence of trauma
10. Palate
11. De-roof blisters if no coagulopathies, blood tests
12. Simplex, dystrophic, junctional, acquisita
13. Clinical descriptive term for full-thickness gingivitis, often with clear distinctions between inflamed and non-inflamed mucosa
14. Erosive lichen planus, mucous membrane pemphigoid, pemphigus vulgaris, erythema (exsudativum) multiforme and lupus erythematosus.
15. Improve OH, SLS-free TP, topical steroids if appropriate, disease control
16. Type III reaction
17. Idiopathic, 50% has a trigger (drugs - carbamazepine, penicillin, NSAIDs), infection, pregnancy, UV, malignancy, chemicals
18. Target lesions - concentric erythematous rings on palms, legs, face, neck, oral lesions (lips, anterior mouth) that are crops of bullae, breakdown into ulcers/erosions, crust and heal in 2 weeks, fever
19. Self-limiting, steroids, acyclovir, fluids, analgesia
20. Steven-Johnson syndrome and TEN
21. High-dose systemic steroids, acyclovir, fluids, analgesia, azathioprine

Question 19

Immunological Diseases 2

1. Clinical appearance of pemphigoid
2. 3 types
3. Aetiology
4. Consequence of undiagnosed cicatritial
5. 4 histological features
6. Management
7. Direct immunofluorescence pattern
8. 3 types of pemphigus
9. Pathogenesis of PV
10. Clinical appearance
11. 4 histological features
12. Management
13. Direct immunofluorescence pattern

Answer 19

1. Thick-walled (full-epidermis/sub-epithelial split) blisters, blood-filled
2. Mucous membrane, cicatricial, bullous
3. Autoimmunity against hemidesmosomes in basal cell layer
4. Scarring of eyes may cause blindness if ocular involvement - oral signs may be warning to prevent ocular damage
5. Sub-epithelial antibody attack (desmoglein destroyed by antibodies, loss of attachment), hemidesmosomes targeted (loss of attachment between basal cell layer and underlying lamina propria and space filled with fluids), full thickness separation of epithelium, no Tzanck cells
6. Steroids, immunomodulators (azathioprine)
7. Linear pattern at basal cell layer (IgG and C3 often present in basement membrane)
8. Vulgaris, IgA, paraneoplastic, familia benign chronic, foliaceus
9. Formation of autoantibodies (IgG, C3) against desmosomes involved in cell-cell adhesion (Dsg-1, Dsg-3), causing intra-epithelial separation above basal cell layer
10. Oedema, intra-epithelial blisters, rupture to leave white friable mucosa, red erosion areas
11. Desmosomes targeted at periphery of spinous cell layer, intra-epithelial separation (supra-basal split - basal cell layer separates from rest of epithelium with lamina propria), tzanck cells, acanthosis
12. Systemic steroids, azathioprine, rituximab (biologics)
13. Basket weave/fisherman’s net pattern

Question 20

PML and Oral Cancer 1

1. Definition of PML
2. Definition of PMC
3. Definition of PMD
4. 4 types of PML
5. Risk of malignant transformation with leukoplakia
6. 3 histological predictors/features of carcinoma
7. Define dysplasia
8. How is dysplasia diagnosed
9. 2 features of mild dysplasia
10. 2 features of moderate dysplasia
11. 2 features of severe dysplasia
12. 2 features of CIS
13. 5 histological features of epithelial dysplasia

Answer 20

1. Altered tissue in which cancer is more likely to form
2. Generalised state associated with increased cancer risk
3. PML and PMD
4. Leukoplakia, erythroleukoplakia, erythroplakia, erosive LP, submocous fibrosis, tertiary syphilis, dyskeratosis congenita
5. 2.5% 10yrs, 4% 20yrs
6. Epithelial dysplasia, architectural changes (abnormal maturation and stratification), cytological abnormalities (cellular atypia)
7. Disordered maturation (growth) in tissue
8. Hyperplasia, mild, moderate, severe, CIS
9. Changes in lower third of epithelium, mild cellular atypia
10. Changes in middle third of epithelium, moderate cellular atypia
11. Changes in upper third of epithelium, severe cellular atypia
12. Malignant but not invasive - abnormal architecture, pronounced cytological atypia
13. Increased and abnormal mitoses (higher position, abnormal form), basal cell hyperplasia, drop-shaped rete pegs, nuclear hyperchromatism, prominent and enlarged nucleoli, disturbed basal cell polarity or loss of cellular orientation, irregular epithelial stratification or disturbed maturation, nuclear and cellular pleomorphism (different size and shape), abnormal keratinisation (below normal keratin layer, keratin pearls), reduced/lost intercellular adhesion

Question 21

PML and Oral Cancer 2

1. 3 high risk sites for OSCC
2. 5 OSCC risk/aetiological factors
3. % risk of synchronous primary with OSCC
4. Briefly describe cancer genetics
5. 5 red flags for OSCC/OPSCC
6. 2 histological patterns of SCC invasive front
7. 3 things that influences prognosis
8. Describe TNM staging system
9. OSCC management options

Answer 21

1. Lateral border tongue, FoM, retromolar trigone, soft palate complex
2. Smoking, alcohol (synergistic), previous SCC, first degree relative with OSCC, poor OH, betel quid, poor diet and nutrition, immunodeficiency, SES, viruses (HPV 16, 18, EBV)
3. 10%
4. Oncogenes, tumour suppressor genes (p53 mutation/inactivation), dysregulation of apoptosis and DNA repair, field change theory
5. Persistent (>2wk) ulcer despite removal of obvious cause, rolled margins, necrotic (firm) centre (indurated, inflamed, granular base, raised edges), speckled leukoplakia, weight loss, dysphagia, worsening pain (neuropathic, dysaesthesia, paraesthesia), referred pain (ear, throat, jaw), cervical lymphadenopathy (enlarged >1cm, firm, fixed, tethered, non-tender)
6. Local, perineurial, lymphatics, haematogenous (lungs, spine, bone). Cohesive or non-cohesive (linked with nodal spread)
7. Site, size, depth of invasion, disease spread, comorbidities, neck metastasis (contralateral and unilateral), ECS
8. T1 - <2cm diameter
   T2 - 2-4cm diameter
   T3 - >4cm diameter
   T4 - >4cm diameter, gross local invasion

N0 - no clinically positive nodes
N1 - single ipsilateral node <3cm
N2a - single ipsilateral node 3-6cm
N2b - multiple ipsilateral nodes <6cm
N2c - bilateral or contralateral nodes <6cm
N3 - any node >6cm

M0 - no distant metastasis
M1 - distant metastasis

9. Surgery, radiotherapy, chemotherapy, immunotherapy
   Curative intent, palliative, best-supportive care

Question 22

Cervical Lymphadenopathy

1. 4 causes of neck lumps
2. Clinical presentation of reactive nodes
3. Clinical presentation of metastatic nodal disease
4. Clinical presentation of lymphoma nodes
5. 2 rarer causes of neck lumps
6. Key features of neck lump exams

Answer 22

1. HNC, infection/reactive (abscess, pericoronitis, tonsilliti, glandular fever), lymphoma, skin swellings, arterial (carotid aneurysm), bone
2. Large (diffuse), tender, inflamed, erythematous surface, soft, mobile, hot
3. Large, firm, fixed, tethered to underlying tissue, non-tender
4. Large, non-tender, rubbery, tethered to underlying mucosa
5. TB, AIDS, Crohn’s, Kawasaki disease, sarcoidosis
6. Site, size, shape, surface, consistency, surrounding anatomy

Question 23

Oral Manifestations of Systemic Diseases 1

1. Aetiology of LP
2. Commonly affected IO sites
3. Skin appearance
4. Difference between LP and lichenoid reaction
5. 4 causes of lichenoid reaction
6. 6 types of LP and clinical appearances
7. 5 histological features of LP/lichenoid reaction
8. Management
9. 2 types of lupus
10. Aetiology
11. Clinical appearance
12. Management

Answer 23

1. Chronic immunological, cell-mediated (type IV) reaction. Autoimmune condition mediated by a T lymphocyte attack on stratified squamous epithelium
2. Buccal mucosa, gingiva, tongue (dorsal/ventral), lips
3. Itchy skin lesions (shiny red/purple papules), interlaced by Wickham’s striae (white lacy lines) on flexor surfaces
4. LP - idiopathic/unknown cause. Tends to present bilaterally
   Lichenoid reaction - identifiable cause. Can present bilaterally, not much more likely to present unilateral
5. Hypersensitivty reaction to amalgam, plaque, SLS, medications (ACE inhibitors, b-blockers, NSAIDs, diuretics, nifedipine)
6. Reticular - bilateral BM. Spider web-like appearance of lacy white lines
   Erosive (ulcerative) - oral ulcers, persistent irregular areas of erythema, ulcers, erosions, covered with yellow slough. Associated with desquamative gingivitis
   Papular - small white asymptomatic pinpoint papules
   Plaque-like - large, homogenous white patches, resembles leukoplakia, common in smokers
   Atrophic - similar to erosive form, associated with desquamative gingivitis, atrophic lesions on background of erythema with radiating white striae at marings
   Bullous - rarer. Fluid-filled vesicles (white or grey/purple, fluctuant) that rupture easily, leave ulcerated surface. Fluid is usually clear but may be haemorrhage or purulent
7. Keratinisation/keratosis of surface epithelium (hyperkeratosis - usually orthokeratosis), acanthosis (hyperplasia of underlying epithelium, especially spinous cells) - elongated rete ridges with saw-tooth appearance, thick sub epithelial ‘hugging’ band of T lymphocytes (blue band of chronic inflammatory cells under epithelium and following contour), occasionally epitheliotropism (inflammatory cells drawn up into epithelial layer), apoptosis (of basal cell layer - cells surrounded by clear halo), destruction of basal cell layer
8. Lichenoid reaction - remove cause, symptomatic relief
   LP - symptomatic relief (benzydamina, SLS-free TP, topical steroids), avoid triggering/spicy/acidic foods. Rarely systemic steroids, azathioprine. Biopsy if suspicious/potentially malignant type. Photos essential
9. CT autoimmune disease. SLE (multi system), chronic discoid (CDLE - limited to skin and mucosa; <50% change of progressing to SLE)
10. Unknown, links to viruses, hormone changes and certain drugs
11. Skin lesions, butterfly zygomatic rash, oral mucosal lesions (palate - ulcers, purport, red/white striae), antinuclear antibodies, arthritis, anaemia
    CDLE - disc-like white plaques IO
12. Topical steroids, DMDs

Question 24

Oral Manifestations of Systemic Diseases 2

1. OFG aetiology
2. Pathogenesis
3. Difference between OFG and (oral presentation of) Crohn’s
4. 6 clinical features
5. 4 histological features
6. Diagnosis
7. Management
8. What does Paget’s affect
9. 2 types and pathogenesis
10. Clinical appearance
11. Radiographic apparence
12. Histological feature
13. What is fibrous dysplasia
14. Clinical appearance
15. Radiographic appearance
16. Histological feature
17. Associated syndrome

Answer 24

1. Type IV (sometimes type I) hypersensitivity to food additives; unknown aetiology.
2. Characterised by non-caseating granulomatous inflammation. Lymphatic obstruction from giant cell granulomas, accumulation of tissue fluid
3. Systemic symptoms. More likely to be Crohn’s If multi-signs are present, particularly linear buccal sulcus ulcers ± sublingual fold stag-horning
4. Angular cheilitis, BM cobblestoning, mucosal tags, aphthous-pattern ulceration (or other types), fistula formation, swollen lips, cheeks and gingivae (full-width gingivitis), gingival erythema, skin changes
5. Non-caseating granuloma formation, giant cell formation, increased tissue fluid production (between CT fibres showing CT fibre separation), lymphatic obstruction and oedema fluid build-up
6. Diagnosis of exclusion, allergy patch test. Avoid cinnamaldehydes and benzoate’s in diet
7. Dietary exclusion, steroids, DMDs, biologics, anti-TNF therapies
8. Skull, pelvis, long bones, jaws
9. Monostotic, polystotic. Replacement of normal bone remodelling by a chaotic alteration of resorption and deposition, with resorption dominating in the early stage
10. Often asymptomatic, frontal bossing, increased hat size, headaches, hearing disturbances
11. Cotton wool appearance, hypercementosis of teeth
12. Increased bone turnover and osteoclastic and osteoblastic activity
13. Slow growing, asymptomatic swelling, active in those <20yrs, area of bone replaced by fibrous CT
14. Monostotic, polystotic
15. Orange peel/ground glass appearance, ill-defined margins between affected and unaffected bone
16. Bone appears as metaplastic or woven, but will remodel and increase in density
17. Albright’s syndrome (melanin pigment, early puberty)

Question 25

Facial Pain 1

Answer 25

1.

Question 26

Facial Pain 2

Answer 26

1.

Question 27

Salivary Gland Disease 1 1. 4 causes of dry mouth 2. Diagnosis of dry mouth 3. 4 symptoms 4. What is a mucocele and how does it appear clinically 5. Aetiology 6. Where does it commonly occur 7. 3 histological features 8. management 9. What is a ranula 10. Clinical appearance 11. Management 12. Necrotising sialametaplasia clinical appearance 13. Pathogenesis 14. 2 risk factors 15. 2 other differentials 17. 3 histological features 18. Management

Answer 27

1. Drugs, alcohol, smoking, radiotherapy, chemotherapy, poorly controlled diabetes, Sjogren's, psychogenic 2. Unstimulated salivary flow rate of <1.5ml in 15mins 3. Swelling difficulties, clicking speech, dysaesthesia/soreness, discomfort, altered taste, non-retentive dentures, (cervical) caries, halitosis 4. Mucus extravasation or retention cyst. Swelling, bluish translucent colour, soft 5. Traumatic (trauma to duct/minor gland) 6. Low lip, palate, BM, tongue, FoM 7. Cystic cavity containing saliva, wall of granulation tissue, macrophage lining. Some macrophages may fall into cavity, engulf saliva and swell 8. Excision with damaged glands and duct 9. Mucus extravasation cyst - Mucocele of major gland (usually sublingual) found on FoM 10. Large bluish, translucent swelling on FoM, may get bigger when eating 11. Excise with associated duct/gland 12. Vascular, usually painless lesion. Swelling then ulceration 13. Small vessel ischaemia followed by necrosis 14, Smokers, trauma, LA 15. OSCC, salivary gland carcinoma 16. Surface slough (necrosis), hyperlplasia of surface epithelium (pseudo-epitheliomatous hyperplasia), squamous metaplasia of ducts, necrosis of salivary acini, inflammation 17. Self-limiting, usually heals within 2-3 weeks. Review and if not healed, consider urgent biopsy

Question 28

Salivary Gland Disease 2 1. 2 types of Sjogren's and differences between them 2. 2 associated CT diseases 3. Diagnosis criteria 4. 3 histological features 5. 2 complications 6. Management 7. Definition of sicca syndrome 8. 3 cause of hyper salivation 9. Clinical appearance of subacute obstruction 10. Management 11. What is sialadenitis 12. Aetiology 13. Treatment 14. What is recurrent parotitis 15. What is Freye's syndrome 16. Treatment

Answer 28

1. Primary - no associated CT disease Secondary - associated CT disease 2. SLE, RA, systemic sclerosis 3. Modified European - 4+ positive criteria including 5 and 6 1 and 2. Dry eyes subjective/objective - dry for >3mths, recurrent sensation of gravel in eyes, tear substitutes >3 times/day 3 and 4. Dry mouth subjective/objective - for >3mths, reduced unstimulated flow rate, liquid to swallow dry food 5. Anti-Ro, anti-La autoantibodies (bloods) 6. Positive labial gland biopsy 4. Minor glands - more than one collection of 50+ lymphocytes within 4mm2 around gland Major glands - lymphocytic infiltration extending to whole lobules, acing atrophy, hyper plastic ductal epithelium 5. NHL, caries, oral infection 6. SF gum, regular water, high F TP, alternative drugs, SLS-free TP, salivary substitutes (salivary orthana, biotene oral balance, bioextra gel), pilocarpine 7. Dry mouth - partial Sjogren's findings 8. Stroke, drugs, MS, Alzheimers, Parkinsons, perceived (swallowing failure, postural drooling) 9. Swelling associated with meals, slowly progressive, eventually fixed and painful. Due to sialoliths or mucous plugging 10. Removal of obstruction/gland 11. Inflammation of major SG 12. Obstruction (stone, stricture) or bacterial (S. aureus) 13. Rehydration, remove obstruction or pus culture and ABX, gland removal 14. Bacterial infection, common in children, resolves by puberty 15. Syndrome involving duct and gland fistula (EO saliva leakage) 16. Botox, excision of duct, gland removal, propantheline before food (reduce salivary flow), scolopaline patches

Question 29

Salivary Gland Disease 3 1. Describe % for where SG neoplasms are likely to occur and % for how likely to be malignant 2. SG symptoms 3. How common is pleomorphic (salivary) adenoma (PSA) 4. Where most likely to occur and 2 histological features 5. Management 6. 2 problems 7. How common is Warthin's and where most likely to occur 8. Management 9. How common are SG carcinomas 10. What are 2 most common types 11. How common are adenoid cystic and where are they most likely to occur 12. How common are mucoepidermoid carcinomas 13. Name 2 other SG carcinomas

Answer 29

1. Parotid - 80% (15% malignant) - 80% in superficial lobe SM - 10% (30% malignant) Minor - 10% (45% malignant) SL - 0.5% (80% malignant) 2. Localised swelling, painless, slow growing, well defined, neuro changes (CNVII involvement) 3. 75% 4. Parotid. Often incomplete capsule, foam cells (macrophages that have engulfed mucin) 5. Wide local excision 6. Recurrence, 5% risk of malignant transformation 7. 15%, parotid 8. Excision 9. 15% 10. Malignant pleomorphic adenoma, carcinoma ex pleomorphic 11. 5%, minor glands 12. 3-5% 13. Acinic cell carcinomas, polymorphous adenocarcinomas, adenoid cystic carcinoma