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Oral Disease > All Oral Disease > Flashcards

All Oral Disease Flashcards

1
Q

When to do a biopsy (5)

A

Confirm diagnosis

Exclude other pathology

When unsure of diagnosis

When we remove a lump

When lesion changes

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2
Q

Types of biopsies (5)

A

Incisional - only part of lesion removed

Excisional - involves removal of whole lesion

Core - usually used for lumps

Fine needle aspiration - not used orally

Smears

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3
Q

Why to do blood tests (4)

A

Check there is no underlying condition leading to oral disease

Monitor the condition

Ensure its safe for patient to have treatment

Monitor it is safe to continue treatment

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4
Q

Types of blood tests (6)

A

Haematology - FBC

Clinical chemistry - Liver and renal profiles

Coagulation - INR

Immunology - Autoimmune profile

Microbiology/virology - HIV syphilis

Special clinical chemistry - tumour markers

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5
Q

Special investigations (6)

A

Imaging - radiographs

Oral rinses, swabs

Sialometry Schirmers - determine how many tears they are producing

Dental - probing, percussion, vitality

Clinical - apply pressure with glass slide on suspected vascular lesion to see blanching

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6
Q

General management strategy for oral disease (3)

A

Aim for the consultation

Short term management

Long term management

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7
Q

What is an incisional biopsy

A

Removal of part of the lesion

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8
Q

What is an incisional biopsy used for

A

Used for large lesions to establish the diagnosis or where treatment depends on the diagnosis

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9
Q

What makes a good incisional biopsy (3)

A

Get both epithelium and underlying tissue

Get some of the lesion and some normal tissue

Full thickness of lesion

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10
Q

What is an excision biopsy

A

Removal of the whole lesion

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11
Q

What is an excisional biopsy used for (2)

A

Management of lesion

Used for small lesions to confirm diagnosis and for more sinister lesions to establish completeness of excision

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12
Q

What is fine needle aspiration used for (3)

A

Obtain cells from deep lesions

For suspected malignancy or cystic lesions

Not appropriate for oral cavity

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13
Q

What is core/needle biopsy used for

A

Obtain a small sample or core of tissue from deep lesion

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14
Q

What are smears used for

A

Examination of cells - fungal infections

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15
Q

What biopsy would be most appropriate

A

Incisional

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16
Q

What biopsy would be most ideal for this lesion

A

Excisional

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17
Q

What would be some differential diagnoses for this lesion

A

Leukoplakia

Candida

Oral cancer

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18
Q

What would be a differential diagnosis for this lesion

A

Polyp

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19
Q

What makes a good microbiology sample (8)

A

Collect specimen prior to administration of antimicrobial therapy

Specimen must be from actual infection site

Collection and transportation is critical - minimising contamination

Prompt processing - pathogens die in transport and delay giving false negatives

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20
Q

What is a transport medium

A

Medium containing no growth supporting nutrients - it aims to maintain viability without supporting growth

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21
Q

What is present in a transport medium (3)

A

Reducing agent - Preserve anaerobes but allows aerobes to survive

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22
Q

Microbiology sampling options for pus (3)

A

Swabs - clean mucosa, incision, send in transport medium

Aspirate - leave in syringe and make needle safe

Paper points - send in transport medium

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23
Q

Options for microbiology sampling for mucosa and skin (2)

A

Swabs - dry site = moisten swab and standard transport medium, suspected viral = viral swab and viral transport medium

Oral rinse - provides info on microbial load (10ml of saline, rinse for 30 seconds and spit in tube)

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24
Q

What is a category A infectious substance

A

One which when exposure to it occurs, is capable of causing permanent disability , life threatening or fatal disease - HIV, Hep B/C, Mycobacterium tuberculosis

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25
Q

What percentage of people will have third molar teeth

A

50%

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26
Q

What percentage of third molar teeth will be impacted

A

20%

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27
Q

What is an impacted tooth

A

One which is prevented from reaching normal position by the presence of other structures - usually adjacent tooth

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28
Q

Common problems associated with third molar teeth (11)

A

Abnormal position

Caries

Periodontal problems

Pericoronitis

Resorption

Cyst formation

Difficulty in OH and food packing

Crowding of lower incisors

Oftern involved in line of mandible fractures

In the way for orthognathic surgery

Potential risk in the future for vulnerable and medically compromised patients

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29
Q

What is pericoronitis

A

Inflammation of soft tissues around the crown of a partially erupted tooth, caused by bacterial infection or trauma

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30
Q

Signs/symptoms of pericoronitis

A

Pain/discomfort

Soft tiisue swelling in region of unerupted tooth

Difficulty eating, swallowing, opening mouth

Tenderness on closing if opposing tooth in contact with inflamed tissue

Unpleasnat taste or smell

Unwell with pyrexia

Reccurent

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31
Q

Signs of pericoronitis (5)

A

Localised intraoral swelling

Evidence of trauma from opposing tooth

Pus +/-

Local lymphadenopathy +/-

Facial swelling +/-

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32
Q

Management of pericoronitis

A

Irrigation beneath gum flab - saline, chlorhexidine

Remove upper 8 if traumatic occlusion

Advise hot salt mouthwash/chlorhexidine/analgesics

Antibiotics - metronidazle 200mg TDS

Drain pus

Review - consider removal if persistent

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33
Q

NICE guidelines in regards to removal of wisdom teeth

A

Routine prophylactic removal of pathology free impacted third molars should be disconinued

Plaque formation is a RF not an indication for removal

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34
Q

Pericoronitis treatment options (4)

A

Observation

Removal

Operculectomy

Coronectomy

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35
Q

Minor complications with third molar removal

A

Pain, swellin, trismus

Infection

Fracture

Bleeding and bruising

TMJ problems

Temporary nerve damage

Periodontal problems

Damage to adj teeth

OAC

Fractured mandible

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36
Q

Major complications with third molar removal

A

Trigeminal nerve damage

Lingual nerve damage

Inferior alveolar nerve damage

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37
Q

Inferior alveolar nerve damage incidence

A

Temporary - 5-7%

Permanent - 0.5-1%

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38
Q

Lingual nerve damage incidence

A

Temporary - 3-7%

Permanent - 0.3-0.5%

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39
Q

Effects of trigeminal nerve damage (5)

A

Complete loss of sensation to half of anterior tongue/chin/lip

Paraesthesia

Dysaesthesia

Alloydina - painful response to painfless stimulus

Loss of taste

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40
Q

Symptoms of nerve injury

A

Pain, unpleaant, burning, tingling

Patient feels they are dribbling

Patient bites lip

Avoid eating in public

Don’t enjoy kissing - allodynia

Bite tongue

Tongue feels like large lump of jelly

Lose food under their tongue

Don’t enjoy food

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41
Q

What is the surgical technique to manage lingual nerve injuries

A

Raise lingual flap and lingual periosteum divided

Central and distal nerves stumps identified and mobilised

Damaged segment of nerve excised

Direct reapposition with sutures

All patients given dexamthasone and antibiotics

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42
Q

How to check if lingual nerve damage surgery was successful

A

Light touch

Pin prick

Two point discrimination

Gustatory response

Altered sensation

Subejctive assesment

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43
Q

How to manage IAN injury following third molar removal

A

Immediate repair at the time of third molar removal

Control bleeding with temporary packing with gauze

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44
Q

Indications for surgical intervention with nerve damage (2)

A

Persistent anaesthesia

Dysaesthesia

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45
Q

What are the types of mucosa (3)

A

Masticatory

Lining

Specialised

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46
Q

Features of masticatory mucosa (4)

A

Pink and stippled

Firmly fixed to underlying bone

Mucoperiosteum

Resists stresses and strains

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47
Q

What type of mucosa is this

A

Masticatory

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48
Q

Histological features of masticatory mucosa (4)

A

Keratin on surface of epithelium (ortho = no nuclei, para = nuclei)

Granular layer present in between keratin and prickle cell layer (dark red)

Reduced submucosa layer known as the mucoperiosteum

Minor salivary glands present of later aspect of palate

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49
Q

Where is masticatory mucosa found (2)

A

Gingivae

Hard palate

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50
Q

Where is lining mucosa found (2)

A

Soft palate

Buccal mucosa

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51
Q

Functions of lining mucosa (2)

A

Loose submucosa - fat in these locations allowing flexibility and movement

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52
Q

Histological features of lining mucosa (3)

A

No keratin on surface

No granular cell layer

Majority is prickle cell layer

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53
Q

What type of mucosa is this

A

Lining

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54
Q

Where do you find specialised mucosa

A

Dorsum of the tongue

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55
Q

What are the types of papillae (4)

A

Filiform

Fungiform

Foliate - lateral aspect

Circumvallate - poster 1/3 border

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56
Q

Function of specialised mucosa (2)

A

Taste buds - fungiform and foliate

Abrasion - filiform

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57
Q

Histological features of specialised mucosa (2)

A

Peaks of keratin - filiform

Muscle beneath the lamina

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58
Q

What type of mucosa is this

A

Specialised

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59
Q

What is leukodema

A

Generalised opacification of buccal mucosa

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60
Q

Which group of people are more likely to have leukodema

A

Afro american

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61
Q

What happens when you apply pressure to leukodema lesions

A

The white lesion disappears however doesn’t rub off

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62
Q

What is the cause of leukodema

A

Unknown - potentially smoking

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63
Q

Histological features of leukodema

A

Vacuolated and oedematous cells in epithelium - gives white appearance

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64
Q

What is this lesion

A

Leukodema

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65
Q

Differential diagnosis for Leukodema (3)

And why it cannot be them

A

White sponge nevus

Chronic cheek biting (frictional keratosis)

Lichen planus

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66
Q

Features of geographic tongue (2)

A

Islands of erythema with white borders

Asymptomatic or mild soreness

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67
Q

Management of geographical tongue

A

Doesn’t necessarily need treatment

Advise against spicy foods

Difflam mouthwash

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68
Q

Differential diagnosis for geographical tongue (2)

A

Frictional keratosis

Lichen planus

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69
Q

What is this lesion

A

Geographic tongue

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70
Q

Features of fordyce spots

A

White or yellow speckling

Asymptomatic

Soft, symmetrically distributed, creamy white spots from 0.5-2mm

On buccal and labial mucosa

More obvious in older patients

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71
Q

What is this lesion

A

Fordyce spots

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72
Q

Features of white sponge naevus

A

Area appears thickened and white clinically due to keratin on surface

Thick, white folds, wrinkled, ebbing tide

Bilateral

Found on cheeks and floor of mouth

Life long

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73
Q

How does white sponge naevus occur

A

Autosomal dominant condition

Point mutation in keratin 4 and 13 which is only found in mucosa thus doesn’t affect skin

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74
Q

Differential diagnosis for White sponge naevus (4)

A

Lichen planus

Lichenoid reaction

Chronic cheek biting - frictional keratosis

Leukoedema

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75
Q

What is this lesion

A

White sponge naevus

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76
Q

What are the age related changes seen in oral mucosa (4)

A

Mucosa may appear atrophic and smoother

Decrease in elasticity therefore not as flexible

Prominence of fordyce spots due to the atrophy of mucosa

Varicosities on ventral surface tongue

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77
Q

What is this lesion

A

No lesion, just age related changes causing varicosities

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78
Q

What can cause trauma to oral mucosa

A

Mechanical - dentures, teeth, orthodtonics appliances, surgical wounds

Chemical - Burns, allergy

Physical - extremes of hot and cold, irradiation

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79
Q

Responses of oral mucosa to trauma

A

Epithelial changes

Connective tissue changes

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80
Q

What is ulceration

A

Loss of the full thickness of epithelium

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81
Q

Histological features of ulcerations

A

Exposure of underlying connective tissue

Pink area seen on top of ulcer is slough - fibrin and neutrophils (makes it appear yellow)

Beneath is granulation tissue - healing tissue where fibroblasts lay down collagen and endothelial cells form new blood vessels

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82
Q

Causes of ulcerations (4)

A

Denture trauma

Chemical burns

Teeth

Irradiation from malignancy

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83
Q

What is this lesion and how was it caused

A

Ulceration caused by trauma

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84
Q

What is this lesion and how was it caused

A

Ulceration caused by chemical burns

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85
Q

What is this lesion and how was it caused

A

Ulceration caused by denture trauma

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86
Q

What is this lesion and how was it caused

A

Ulceration caused by biting tongue

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87
Q

What is keratosis

A

Keratinisation where there wouldn’t usually be keratin present

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88
Q

What is hyperkeratosis

A

Extra keratosis where there would be keratin usually

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89
Q

What is atrophy

A

Reduction in thickness of epithelium due to loss of cells

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90
Q

What is hyperplasia

A

Overgrowth of connective tissue

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91
Q

What happens in hyperplasia (3)

A

Body produces more collagen as an immune response

Fibroblasts producing excess collagen

Sometimes pedunculated (stalk), or cecile (flat)

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92
Q

What is frictional keratosis and where is it found

A

White patch caused by continual trauma along the occlusal line or opposite sharp cusps, ortho wires or dentures

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93
Q

How to diagnose frictional keratosis

A

Must be able to demonstarte lesion caused by trauma

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94
Q

Management of frictional keratosis

A

Remove cause

Biopsy if it doesn’t regress

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95
Q

Features of Stomatitis nicotina

A

Diffused white patch on hard palate

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96
Q

What is stomatitis nictonia caused by

A

Use of pipe and cigars - thermal heat

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97
Q

Stomatitis nicotina treatment (3)

A

Stop and reduce smoking

Regular review

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98
Q

What is this lesion

A

Frictional keratosis

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99
Q

What is this lesion

A

Stomatitis nicotina

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100
Q

What is papillary hyperplasia of palate caused by

A

Ill fitting dentures - body responds by forming polyps

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101
Q

Features of papillary hyperplasia of palate (3)

A

Symptomless

Erythematous overgrowth of mucosa

Corresponds to denture outline

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102
Q

Management of pappilary hyperplasia of palate (2)

A

New dentures

Excision

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103
Q

What is primary intention

A

Wound is sealed with stitch

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104
Q

What is secondary intention

A

Wound is not sealed up

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105
Q

Factors affecting healing (8)

A

Primary or secondary intention

Foreign body

Vascular supply

Nutritional deficiencies

Irradiation

Malignancy

Infection

Poor immune response

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106
Q

What is Fibrous hyperplasia

A

Overgrowth of fibrous connective tissue

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107
Q

What is another name for fibrous hyperplasia

A

Fibroepithelial polyp

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108
Q

What epithelium would you find at a fibrous hyperplasia lesion

A

Hyperkeratinised stratified squamous epithelium

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109
Q

Management for fibrous hyperplasia

A

Excision, remove cause, send for histopathological examination

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110
Q

Features of fibrous hyperplasia (5)

A

Pedunculated or cecile

Same colour as normal mucosa

Firm

Painless unless traumatised

Main site - buccal mucosa along occlusal plane or lip at sites of biting

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111
Q

Causes of fibrous hyperplasia (3)

A

Trauma

Dentures

Orthodontic appliances

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112
Q

What is a pyogenic granuloma

A

Benign proliferation of capillary blood vessels caused by trauma, found anywhere in the oral cavity

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113
Q

Features of a pyogenic granuloma (6)

A

Red/blue/purple vascular growth

Cecile or pedunculated

Rapid growth

Soft

Bleeds easily

Common in pregnancy

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114
Q

Management of a pyogenic granuloma (2)

A

Excision and remove cause

If pregnant, improve OH and excise but may recur

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115
Q

What is this lesion

A

Fibrous hyperplasia/fibrous epithelial polyp

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116
Q

What is this lesion

A

Pyogenic granuloma

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117
Q

What is this lesion

A

Fibrous hyperplasia

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118
Q

What is a peripheral giant cell granuloma

A

A benign slow growing lesion which contains multinucleated osteoclasts and giant cells, and lies within the gingiva

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119
Q

Features of a peripheral giant cell granuloma (8)

A

Soft red/blue cecile or pedunculated swelling

Usually anterior teeth, mandible>maxilla

Only on gingiva

Haemorrhage

May cause superficial bone resorption

Numerous multinucleated giant cells

Clinically same as pyogenic granuloma

Histologically same as giant cell lesion

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120
Q

Peripheral giant cell granuloma Management

A

Determine origin and extent of lesions - Gingiva or bone

Excision, curettage of underlying bone and histopathological examination

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121
Q

What is this lesion

A

Peripheral giant cell granuloma

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122
Q

What are Bohn’s nodules

A

Embryologic remanence of when palatal shelves fused leaving trapped epithelium and epstein pearls

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123
Q

Features of Bohn’s nodules (4)

A

Cysts of epithelium filled with keratin - appears white

Always found in the midline of palate

Maybe one or multiple present

Spontaneously disappear

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124
Q

What is this lesion

A

Bohns nodules

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125
Q

If a lesion is firm, mucosa coloured, what could it be

A

Fibrous hyperplasia

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126
Q

If a lesion is soft, red, red/blue, what could it be

A

Pyogenic granuloma

Giant cell granuloma

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127
Q

If patient is pregnant and has an oral mucosa lesion, what could it be

A

Pyogenic granuloma

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128
Q

What should you do confirm diagnosis for an oral mucosa swelling

A

Excisional biopsy

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129
Q

Localised gingival swellings (5)

A

Fibrous hyperplasia

Pyogenic granuloma

Peripheral giant cell granuloma

Gingival cysts

Bohns Nodules

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130
Q

Generalised gingival swellings (7)

A

Hereditary - gingival fibromatosis

Inflammatory - Chronic hyperplastic gingivitis

Hormone related - endorcrine related

Diet related - scurvy

Neoplastic - Leukemic infiltration, Wegener’s granulomatosis

Drug related - drug induced gingival hyperplasia

Associated with GI tract disease - Crohns

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131
Q

Features of gingival fibromatosis (4)

A

Hereditary - autosomal dominant

Lifelong

Pale pink and firm overgrowth

Looks like polyp but all over the gum

May cover and submerge teeth

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132
Q

Treatment for gingival fibromatosis

A

Gingivectomy, but may regrow after removal

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133
Q

What is this lesion

A

Gingival fibromatosis

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134
Q

Features of chronic hyperplastic gingivitis (2)

A

Associated with poor OH

Erythematous gingivae, bleeding on probing

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135
Q

Features of endocrine related generalised gingival swellings (3)

A

Related to pregnancy/puberty

Exuberant response to plaque

Red, erythematous, bleeds easily on probing

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136
Q

Features of diet related generalised gingival swellings (4)

A

Vit C deficiency

Failure to synthesise collagen

Loss of teeth due to loss of periodontal support

Inflammatory type hyperplasia

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137
Q

What is this lesion

A

Diet related generalised gingival swelling

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138
Q

Features of gingival hyperplasia associated with leukaemia (8)

A

Red, swollen gingivae

Pus

Ulceration

Response in excess of amount of plaque

Petechial haemorrhages, tiredness

Area of necrosis

Rapidly progressing

Especially concerning in children

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139
Q

Features of drug induced gingival hyperplasia (4)

A

Gingivae is pale, lobulated

Little inflammation

Dense fibrous tissue

Long epithelium rete ridges

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140
Q

Management of drug induced gingival hyperplasia

A

Surgical reduction

Improve OH

Change drug regime if possible

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141
Q

What is drug induced gingival hyperplasia associated with (3)

A

Cyclosporin

Nifedipine

Phenytoin

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142
Q

Features of GI tract associated generalised gingival swellings (4)

A

Labial swelling

Apthous ulcer

Cobblestoning on buccal mucosa

Granulomas

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143
Q

If a generalised gingival swelling is pale and the gingivae is uninflamed, what would it be

A

Gingival fibromatosis

Drug induced

Differentiate by drug history and duration

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144
Q

If a generalised gingival swelling is red and the gingiva is inflamed, what could it be

A

Inflammatory hyperplasia

Hormone induced

Differentiate by history

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145
Q

If a generalised gingival swelling is red, inflamed, exudating pus and ulcerated, what could it be

A

Leukaemia

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146
Q

What is a squamous cell papilloma

A

Benign neoplasm (overgrowth of hyperkeratinised epithelium) associated with the HPV (6 and 11)

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147
Q

Features of a squamous cell papilloma (6)

A

White cauliflower like growth

Pedunculated or cecile

Common on palate

Surface thrown into fronds

Vascular connective tissue core

Low virulence

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148
Q

Management of squamous cell papilloma

A

Excision with a margin

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149
Q

What is this lesion

A

Squamous cell papilloma

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150
Q

What is Heck’s disease

A

Also known as focal epithelial hyperplasia

Multiple papillomas caused by HPV 13 and 32

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151
Q

Features of hecks disease (5)

A

Multiple papillomas - cobblestone look

Caused by HPV 13 and 32

Asymptomatic

Multiple flat viral warts

Occurs in childhood

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152
Q

Management of Heck’s disease

A

May resolve spontaneously

Excise

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153
Q

What is this lesion

A

Hecks disease

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154
Q

What is a traumatic neuroma

A

Haphazard overgrowth of nerve fibres caused by trauma (common in mental foreman region)

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155
Q

What is a lipoma

A

Benign neoplasm composed of fat

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156
Q

Features of a lipoma (5)

A

Yellow/pink

Smooth surface

Asymptomatic

Common check and tongue

Composed of fat

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157
Q

Management of lipoma

A

Excision

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158
Q

What is the malignant form of lipoma

A

Liposarcoma

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159
Q

What is this lesion

A

Lipoma

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160
Q

What is a haemangioma

A

Excess of blood vessels

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161
Q

What is a hamartoma

A

Abnormal peripheralisation of normal tissues for that site

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162
Q

What is choristoma

A

Pheripheralisation of tissue but tissue is abnormal for that site

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163
Q

Features of a haemangioma (6)

A

Appears soon after birth then disappears when older

Excess blood vessels

Blue/purple in colour

Localised or diffuse

May bleed excessively

If pressure applied adjacent = blanching

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164
Q

What is this lesion

A

Haemangioma

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165
Q

What is sturge weber syndrome

A

Neurological condition that is present from birth and is distributed along one or more branches of the trigeminal nerve

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166
Q

Features of sturge weber syndrome (4)

A

Port wine stain

Varying degrees of mental retardation

Seizures

Glaucoma

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167
Q

What is this lesion

A

Sturge weber syndrome

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168
Q

What is a mucocele

A

Collection of saliva in a benign cyst

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169
Q

Features of a mucocele (5)

A

Collection of saliva

Mucous extravasation cyst

Usually on lower lip after biting

Fluctuant

Clear appearance

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170
Q

Management of a mucocele

A

Excisional

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171
Q

What is a lymphangioma

A

Overgrowth of lymphatic vessels, pale in colour

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172
Q

Features of a neural tumour (3)

A

Deep seated

Relatively rare

Firm and mucosal coloured

Neurofibroma/Neurilemmona

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173
Q

What is this lesion

A

Mucocele

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174
Q

What is this lesion

A

Lymphangioma

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175
Q

What is a granular cell tumour

A

Soft tissue tumour originating from schwann cells

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176
Q

Features of a granular cell tumour (3)

A

Swelling on dorsum of tongue

Containing granular cells thought to have neural origin

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177
Q

Treatment for granular cell tumour

A

Excision

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178
Q

What is congenital epulis

A

Soft tissue tumour arising from schwann cells in neonates

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179
Q

Features of congenital epulis (2)

A

Similar histologically to granular cell tumour

Occurs in neonates

Anterior maxilla on alveolar ridge

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180
Q

Treatment for congenital epulis

A

Excision

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181
Q

Salivary gland tumours are…

A

Benign or malignant

Most common on palate are pleomorphic adenoma

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182
Q

If a lesion is cauliflower like and white, what could it be

A

Squamous cell papilloma

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183
Q

If a lesion issmooth, mucuosal coloured, related to denture or trauma, what could it be

A

Fibrous hyperplasia

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184
Q

If a lesion is yellow and smooth, what could it be

A

Lipoma or abscess

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185
Q

If a lesion is red and white, related to trauma, what could it be

A

Pyogenic granuloma

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186
Q

If a lesion is red or blue, what could it be

A

Haemangioma

Mucocele

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187
Q

If a lesion is deep seated and normal mucosa, what could it be

A

Neuroma

Neural tumour

Salivary gland tumour

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188
Q

What are the phases of tooth eruption (5)

A

Pre eruptive movement - follicle

Intraosseous movement - follicle

Mucosal penetration

Pre occlusal movement

Occlusal function

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189
Q

Systemic factors causing delayed eruption (5)

A

Obstacles - Gingival fibromatosis, Cherubism, gorlin syndrome, Cleidocranial dysplasia, Pierre robin syndrome

Genetic factors - Downs syndrome

Amelogenesis imperfecta

Mucopolysaccharidosis

Endocrine disease

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190
Q

Local factors causing delayed eruption (12)

A

Retention of deciduous predecessor

Premature loss of deciduous tooth

Loss of space

Crowding

Supernumerary or supplemental teeth

Scar tissue

Compact bone

Eruption cyst

Dentigerous cyst

Odontomas

Odontogenic tumours

Fibromatosis

Ankylosis

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191
Q

Signs and symptoms of delayed tooth eruption (6)

A

Failure to erupt as expected

Over long retention of deciduous predecessor

Proclination of adjacent teeth

Loosening of teeth

Pain

Swelling

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192
Q

Most common teeth that fail to erupt

A

8s

Maxillary canines

Mandibular 5s

Upper lateral incisors

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193
Q

Problems with unerupted teeth (6)

A

Cyst formation

Resorption of adjacent teeth

Pericoronitis

Eruption later under a denture or bridge

Hypercementosis

Internal resorption

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194
Q

Treatment of unerupted maxillary canines (5)

A

No treatment

Extraction of deciduous canine

Surgical removal

Surgical exposure

Surgical/Autotransplantation

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195
Q

What is an allergy

A

When the immune system responds in an exaggerated or inappropriate way to an extrinsic (non self) antigen

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196
Q

What is autoimmunity

A

When the immune system responds in an exaggerated or inappropriate way to an intrinsic (self) antigen

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197
Q

What is hypersensitivity

A

When the immune system responds in an exaggerated or inappropriate way resulting in harm

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198
Q

Dental material allergies

A

Orthodontics - nickel containing wires, bracket adhesives, acrylic materials

Restorative - amalgam, composite, denture bases

Plastics - denture acrylic, cold cure acrylics, bonding agents

Metals - mercury, nickel

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199
Q

Features of a macule (3)

A

Circumscribed flat lesion

Not elevated

Not palpable

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200
Q

Features of a papule (3)

A

Circumscribed raised lesion

Raised

Palpable

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201
Q

Features of a blister (2)

A

Fluid filled sac

Within or below epithelium

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202
Q

Features of a vesicle (1)

A

Small bister less than 5mm diameter

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203
Q

Features of a bulla (1)

A

Large blister more than 5mm in diameter

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204
Q

Features of erosion (3)

A

Marked thinning/partial loss of epithelium

Thin epithelial covering of CT

Red and sensitive

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205
Q

Features of an ulcer (3)

A

Localised loss of entire thickness of epithelium

Exposes underlying CT

Usually painful

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206
Q

Mucocutaneous diseases (4)

A

Autoimmune bulbous diseases - type 2 hypersensitivity (pemphigus, pemphigoid, dermatitis herpetiformis)

Epidermolysis bullosa congenita

Erythema multiforme - Type 3, 4

Oral lichen planus and lichenoid reactions - type 4

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207
Q

Pemphigus incidence rate and target audience

A

0.5-3.2 per 100,000

40-60 year olds

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208
Q

Oral features of pemphigus (4)

A

Mouth involved

Palate, buccal mucosa, gingivae most commonly affected

Bullae are short lived in mouth and on skin

Large shallow non healing ulcers

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209
Q

Pemphigus pathogenesis (3)

A

Autoantibody binds to desmoglein 3

Leads to epithelial cell separation (acantholysis)

Formation of an intraepithelial bulla

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210
Q

What is Nikolsky’s sign

A

Identify a normal/healthy looking mucosa in mouth of patient with suspected pemphigus

Rub blunt side of probe on this area

Blister formation on pressure suggests pemphigus

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211
Q

Special investigations for pemphigus (5)

A

Biopsy of para lesion and normal tissue but not blister

Send tissue to lab fresh or frozen not fixed

Routine histology

Direct immunofluorescence

Blood sample

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212
Q

Pemphigus subtypes (3)

A

Pemphigus vulgaris

Pemphigus foliaceus

Paraneoplasric pemphigus

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213
Q

Pemphigus management (4)

A

Exclude cancer

Immunosuppression

Prednisolone alone or in combination with azathioprine

Occasionally other immunosuppressants or plasmapheresis

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214
Q

Pemphigus effects (5)

A

Intra epithelial bullae present covering partial thickness of the epithelium

On rupturing, basal epithelial cells remain

No stimulus to heal

Epithelial permeability barrier is lost

Thus allowing infections to enter, loss of tissue fluid = life threatening

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215
Q

Pemphigoid effects (3)

A

Subepithelial bullae present covering full thickness of epithelium

On rupturing, exposed connective tissue

Healing by secondary intention - epithelial migration from edges, wound contraction, not as life threatening as pemphigus

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216
Q

Pemphigoid pathogenesis

A

Autoantibodies directed against components of the hemidesmosomes - structures fluing the epithelial cells to the basement membranes

Targeted hemidesmosome varies between different types of pemphigoid

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217
Q

Features of bullous pemphigoid (4)

A

Skin usually involved with bullae

Large shallow ulcers or erosions

Mouth and other mucous membranes frequently involved

Autoantibodies directed against the BP180 and BP230 antigens in hemidesmosomes

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218
Q

Histological features of bullous pemphigus

A

Epithelium spearates from CT at the level of basement membrane

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219
Q

Features of mucous membrane pemphigoid (5)

A

Desquamative gingivitis

Buccal mucosa and palate often involved

Eyes severely damaged by scarring (cicatricial pemphigoid)

Skin lesions are rare in MMP

Autoantibodies directed against BP230, laminin, alpha 6 beta 4 in hemidesmosomes

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220
Q

Histological features of mucous membrane pemphigoid

A

Epithelium separates from CT at the level of the basement membrane

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221
Q

Key characteristics of mucous membrane pemphigoid (6)

A

Well defined ulcers

Healing in 3-4 weeks

Risk of scarring eyes, larynx, oesophagus

Erythematous, friable, tender gingiva

Nikolsky sign positive

Conjunctival lesions common

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222
Q

Treatment for mucous membrane pemphigoid (4)

A

Steroids

Plaque reduction

Tetracycline/nicotinamide

Other immunosuppressive agents

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223
Q

Management of mucous membrane pemphigoid (2)

A

Immediate referral (phone)

Needs ophthamology opinion

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224
Q

Special investigations for pemphigus (4)

A

Biopsy of para lesional and normal tissue

Send tissue to lab fresh or frozen - do not fix

Routine histology

Immunofluorescence

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225
Q

Features of dermatitis herpetiformis (2)

A

Smaller bullae and vesicles

Association with coeliac disease

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226
Q

Histological features of dermatitis herpetiformis (3)

A

Small regions of epithelial separation at the level of the basement membrane

Neutrophils/eosinophils - abscesses

Mixed inflammation in CT

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227
Q

What you would expect to see in immunofluorescence of dermatitis herpetiformis

A

Speckled/granular IgA immunofluorescence at the basement membrane and in the adjacent conective tissue

228
Q

Management of dermatitis herpetiformis (2)

A

Gluten free diet

May respond well to antimicrobials such as sulfonamides or dapsone

229
Q

What is Epidermolysis bullosa congenita

A

Genetic defects in key proteins associated with epithelial integrity or anchoring to the CT

230
Q

Different forms of epidermolysis bullosa congenita

A

EB simplex - within epithelium

EB junctional - under epithelium above CT

EB dystrophica - under basement membrane above CT

231
Q

Features of Erythema multiforme (type 3/4) (7)

A

Acute onset

Short duration - 2/3weeks

Mucocutaneous blistering disorder

Peak age range = 20-30 years

Complex pathogenesis

Immune complex mediated sometimes

Some reccurent cases type 4 hypersensitivity to herpes antigens

232
Q

Clinical features of Erythema multiforme (4)

A

Oral - haemorrhagic crusting of lips, extensive irregular mucosal ulceration erythema and blistering

Ocular - conjunctivitis

Skin - “Target” lesions

Severe cases - Stevens Johnson syndrome

233
Q

Causes of eythema multiforme

A

Single - Drugs (carbamazepine, penicillin, NSAIDs), infection (HSV, Mycoplasma pneumonia), Radiotherapy, Idiopathic

Recurrent - recurrent herpes simplex

234
Q

Management of erythema multiforme (8)

A

Remove trigger

Short, reducing dose course of steroids

Chlorhexidine/benzydamine mouthwash

Gengigel/Gelclair

Analgesics

Soft diet

May require admission for parenteral nutrition and more intensive therapy

Recurrent - provide prevention with systemic acyclovir

235
Q

Features of oral lichen planus (5)

A

Cell mediated autoimmune condition

Stress may exacerbate it

Chronic

Difficult to treat

Premalignant (1.5% risk of change)

236
Q

Clinical presentations of lichen planus

A

Reticular - lace like pattern, white striation

Plaque like - not as well defined as reticular

Erosive

Desquamative gingivitis - not the only presentation, lesions will be found elsewhere

Ulcerative

Bullous

237
Q

Skin involvement in lichen planus

A

<10% of patients presenting with oral lesions have skin lesions

50% of patienst presenting with skin lesions have oral lesions

Violaceous, itchy papules and Wickhams striae

Lesions particularly occur on flexor surface of wrists and on shins

238
Q

Types of lichen planus (4)

A

Cutaneous

Genital

Anal

Oesophageal

239
Q

Histological features of lichen planus (3)

A

Band of lymphocytes close to the epithelium

Keratinised therefore white thickness

Thin and vascular epithelium

240
Q

Pathogenesis of lichen planus (6)

A

Band like accumulation of T lymphocytes

Disruption of the basement membrane basal cells

T cell invasion of the epithelium

Damage to the basal cells stimulates an attempt to repair

If rate of damage exceeds rate of repair = thinning of epithelium (atrophic/erosive)

If rate of repair exceeds rate of damage = thickening of epithelium, marked keratinisation (reticular/plaque like)

241
Q

Why are basal keratinocytes targeted for cell mediated autoimmune damage (2)

A

Because keratinocytes start to express altered self antigen

Or because cytotoxic T cells fail to recognise the keratinocytes as ‘self’

242
Q

Treatment for Oral lichen planus (5)

A

Symptomatic relief

Topical analgesics - benzydamine hydrochloride

Topical corticosteroids - beclomethasone, prednisolone, fluticasone

Topical immunosuppressants - retinoids, cyclosporin mouthwash

Systemic immunosuppressant - prednisolone, azathioprine, retinoids

243
Q

What is a lichenoid reaction

A

Lesions that look like oral lichen planus clinically and histologically, but have a known antigenic cause

244
Q

Causes of lichenoid reaction (4)

A

Graft vs host disease - bone marrow transplant (T cells are from donor which can cause the keratinocytes to be recognised as foreign and become damaged)

Contact sensitivity to dental materials - amalgam

Systemic drugs - antihypertensives, antimalarials, anti inflammatories, diabetes treatment

Systemic lupus erythematosus/Discoid lupus erythematosus

245
Q

Management of lichenoid reaction (2)

A

Remove or treat underlying cause - replace filling, change meds

Treat as OLP

246
Q

OLP summary

A

Bilateral

Symmetrical

May involved gingivae or skin

No strong relationship to fillings or drugs

247
Q

OLR summary

A

Unilateral

Asymmetrical

Dont involved gingivae or skin

Closely related to the cause

248
Q

What is this lesion

A

Pemphigus

249
Q

What is this lesion

A

Mucous membrane pemphigoid

250
Q

What is this lesion

A

Erythema multiforme

251
Q

What is this lesion

A

Reticular lichen planus

252
Q

What is this lesion

A

Erosive lichen planus

253
Q

What is this lesion

A

Ulcerative lichen planus

254
Q

What is this lesion

A

Lichenoid reaction

255
Q

What is oral dysaesthesia

A

Describes painful burning feeling in the mouth

256
Q

Aetiology of oral dysaesthesia

A

Unknown

257
Q

Oral dysaesthesia associations (5)

A

Diabtes

Anaemia

B12 and folate deficiency

Candida

Post menopausal women

258
Q

Management of oral dysaesthesia (4)

A

CBT improved in 6 months

Oestrogen improved taste

Alter meds

Correct deficiencies

259
Q

What is trigeminal neuralgia

A

Chronic pain condition that affects the trigeminal nerve, which carries sensation from your face to your brain

260
Q

Presentation of trigeminal neuralgia (8)

A

Patient can bare talk

Wont be able to shave on one side

Cant clean side on one side

Hair wont be kept on one side

Not have been able to eat properly for days

Eating and drinking with straws

Excrutiating pain

Moving away when coming to examine them

261
Q

Features of atypical facial pain (5)

A

Present daily and persist for most or all of the day

Should be confined at onset to a limited area of one or both sides of face, may spread to wider areas

Should not be associated with sensory loss or other physical signs

Laboratory investigations should not demonstrate relevant abnormalities

The pain may be initiated by trauma, but persist without any demonstrable local cause

262
Q

What is atypical odontalgia

A

Severe throbbing pain in the tooth without major pathology, not resolved by RCT, XLA

263
Q

Aetiology of atypical odontalgia (5)

A

Sensitisation of nerves may occur after infection, extraction or even RCT

Changes within the CNS and possibly ongoing neural activity

Female prevalence

Tends to be older patients

Psychosocial factors

264
Q

Causes of oral dysaesthesia

A

Local - bacterial, fungal, allergy, geographic tongue, parafunction, oesophageal reflux, xerostomia

Systemic - Decreased levels of iron, folate, b12, diabetes, menopause, psychogenic, cancerphobia

265
Q

What is hyperalgesia

A

Stimulation is more painful than perceived

266
Q

What is allodynia

A

Non painful stimuli is painful

267
Q

What is spontaneous pain

A

Pain in the absence of a stimuli

268
Q

Signs of acute inflammation (6)

A

Swelling

Redness

Pain or tenderness

Heat

Loss of function

Pyrexia, malaise, lymphadenopathy

269
Q

What is an abscess

A

Pus filled pathological cavity, which can form as part of the inflammatory response to an acute infection

270
Q

How to identify an abscess, cellulitis, oedema

A

Gentle palpation

If soft and fluctuant = abscess

If hard and not fluctuant = cellulitis, no pus

If soft and not fluctuant = oedema

271
Q

Treatment of acute infection - General measures (5)

A

Hospital admissions if unwell

IV fluids, antibiotics, pain relief

Drainage

NSAIDS - pain relief

Antibiotics - blindly (amoxicillin and metronidazole)

272
Q

Treatment of acute infection - Local measures (4)

A

Removal of cause

Drainage

Prevention of spread - drainage, antimicrobials

Restoration of function

273
Q

Aetiology of dentoalveolar abscess (4)

A

Black pigmented anaerobes

Anaerobic cocci

Non pigmented anaerobes

Spirochaetes

274
Q

Symptoms of periodontal abscess (4)

A

Pain

Swelling

Lymphadenopathy

Facial or neck cellulitis

275
Q

Features of a peridontal abscess (3)

A

Radiolucency on lateral aspect of the root

Multiple periodontal abscesses seen in poorly controlled diabetic patients

Microbial aetiology is same as chronic periodontitis plus candida

276
Q

Treatment for periodontal abscess

A

Drain and debride

277
Q

Features of streptococcal gingivostomatitis (4)

A

Rare in non compromised hosts - frequently follows tonsillitis

Severe inflammation of the gingivae with marked pain

Caused by S.pyogenes - complications = fascilitis, tissue destruction, rheumatic heart disease, nephritis

Treat with penicillin promptly

278
Q

Features of acute ulcerative gingivitis

A

Usually due to poor oral hygiene, smoking, stress

Ulceration and destruction of interdental papilla

Halitosis, malaise, lymphadenopathy

Bacteria - Treponema vincentii, fusobacterium, Prevotella intermedia

279
Q

Features of cancrum oris noma (4)

A

Usually preceded by ANUG and recent debilitating illness - infection, immunosuppressive drugs/disease, malnutrition

F.necrophorum, P.intermedia, T.vincentii, T.denticola, T.forsythia

90% mortality rate

Mainly affects children under 12 in africa and west India

280
Q

Features of tuberculosis

A

Rare in oral cavity - secondary to pulmonary presentation, cough, cervical lymphadenopathy, ulceration, delayed healing of teeth following extraction

281
Q

Features if primary syphilis (5)

A

Chancre on lip or tongue

Ulcer, local oedema painless

Lymphadenopathy

Smear shows spirochaetes

Causative organism is treponema pallidum

282
Q

Features of secondary syphilis (4)

A

Around 6 weeks after healing of primary lesion

Snail track ulcers

Lymphadenopathy

Skin rash usually on palms of hands and soles of feet

283
Q

Features of tertiary syphilis (3)

A

Rarely seen in western world

Gumma (lump of soft tissue) on palate, tongue, tonsil - firm, necrotic, centre surrounded by inflammed tissue

Leukoplakia (white patch) on dorsum of tongue and increased incidence of oral cancer

284
Q

Features of congenital syphilis (2)

A

Child infected in utero

Leads to distinctive dental morphology - Hutchinsons incisors (notch on incisal edge) and mulberry molars (multiple rounded rudimentary enamel cusps on first permanent molars)

285
Q

Features of gonorrhea (4)

A

Pharynx and any part of oral mucosa can be affected

Pain and lymphadenopathy

Variable appearance - ulceration, oedema, pseudomembranes growing over ulcers

Direct examination of smear or culture necessary

286
Q

Features of actinomycosis (2)

A

Slow growing extraoral swelling at corner of mandible - sometimes following traumatic extraction of wisdom teeth)

Actinomyces israwlii, A.oris, A.naeslundii

287
Q

Histological features of actinomycosis (2)

A

Highly branched gram positive filamentous organisms

Locules of pus surrounded by fibrous septa

288
Q

Treatment for actinomycosis (2)

A

Surgical drainage and debridement

Antibiotics for 6-8 weeks (won’t work alone as they cannot access walled off necrotic avascular area)

289
Q

Features of acute bacterial sialadenitis (4)

A

Ascending infection - mainly parotid

Usually due to failure of secretion - sjogrens syndrome, gland pathology, sialolithiasis, drugs

Unilateral, firm, red swelling, extreme pain, trismus, possibly febrile, milking duct releases pus

Microbial causes - oral steptococci, oral anaerobes, Staphylococcus aureus

290
Q

Treatment for acute bacterial sialadenitis (2)

A

Amoxicillin, Flucloxacillin

Sialography after resolution and possible surgical exploration

291
Q

Causes of angular cheilitis (3)

A

Seen in denture wearers - poor denture hygiene

Haematological deficiency - iron, b2,3,6,12

Candida sp., Staph.aureus - alone or mixed

292
Q

Treatment for angular cheilitis (3)

A

Miconazole - Candida albicans

Nystatin - Candida glabrata

Fusidic acid

293
Q

Complications of orofacial infection (5)

A

Airway - Obstruction due to oedema/swelling, aspiration

Vascular - venous thrombosis, carotid blowout

Osteomyelitis

Mediastinitis

Swelling, fever, malaise = antibiotic support needed

294
Q

When are antibiotics indicated (6)

A

Systemic symptoms present

Spreading infection

Chronic infection despite drainage

Immuno or medically compromised

Conditions difficult to resolve without or that speed up recovery

When local measures not worked

295
Q

How to use antimicrobials (3)

A

Must be aimed at the organism present

Dose must achieve 4-8 times minimal inhibitory concentration in blood

Must be present long enough to penetrate adequately to the site, but not too long as will contribute to antimicrobial resistance

296
Q

What to consider when selecting an antimicrobial agent

A

Broad spectrum agents - associated with rise in other diseases such as C.difficile disease

Empirical use

Don’t prescribe for pulpitis, prevention of dry socket

297
Q

Reasons why antibiotics fail (4)

A

Agent does not reach the site - poor blood supply, inadequate drainage, presence of a foreign body, inadequate duration

Impaired defences - immunocompromised

Inappropriate agents can lead to resistance

Poor patient complaince

298
Q

Features of Temporal arteritis (giant cell arteritis) (6)

A

New persistent headache - frontal and occipital

Autoimmune - T cells attack internal elastic lamina, inflammation clogs up lumen of artery, less blood can get through, ischaemia and claudication

Swollen tender scalp artery with elevated ESR or CRP

Temporal artery biopsy demonstrating arteritis

Major improvement within 3 days of steroid therapy

Associated with polymyalgia rheumatica

299
Q

Presentation of temporal arteritis (7)

A

Usually elderly - 50 years old

New onset headache

Pain on mastication

Scalp tenderness

Generally unwell

Tenderness or decreased pulsation of temporal vessels

Elevated ESR >50mm/h

300
Q

Pathology of temporal arteritis (4)

A

Inflammation and necrosis of arterial media wall

Infiltrate of CD4 T cells, lymphocytes, macrophages, multinucleated giant cells

Infectious agents involved in pathogenesis - VZV implicated but not proven

Genetic predisposition (HLA), but results cant be replicated

301
Q

Management of temporal arteritis (4)

A

50% have involvement of opthalmic artery = blindness

Should be treated as emergency as blindness cannot be reversed

Steroids (prednisolone) may be reverse inflammation - decreased vision (not blindness) (Visual symptoms = 80mg initially, No visual symptoms = 60mg initially)

Urgent referral to either GMP, rheumatology, opthamology

302
Q

Features of a cluster headache (5)

A

Unilateral pain

Principally in ocular, frontal and temporal areas

Recurring, daily attacks for several months

Usually rhinoorhea and lacrimation

Severity comparable with trigeminal neuralgia

303
Q

Management of cluster headaches (2)

A

Acute attack - oxygen, 100% 10-12L/minute, Sumatriptan

Prevention - Avoid precipitating factors (alcohol, coffee)

304
Q

What are migraines

A

Episodic headache usually accompanied by nausea, photophobia, phonophobia

305
Q

Features of migraines (4)

A

Duration - 4-72 hours

Pulsating pain usually unilateral

Aura in 15% of patients

Triggers - hormonal, relaxation, perfume, stress, oestrogen

306
Q

Treatment for migraine (3)

A

Simple analgesia - ibuprofen, paracetamol

5HT1 agonist - triptan

Antiemetics - metoclopramide

307
Q

Prevention of migraines (6)

A

Prescription if patient has over 2 per week

Interferes with daily function

Medications do not control pain - amitriptyline, beta blocker, pizotifen

Patient education

Psychological

TENS/acupuncture

308
Q

Signs/symptoms of Masticatory muscle disorders (3)

A

Local myalgia

Myofascial pain

Myofascial pain with referral

309
Q

Signs/symptoms of temporomandibular joint disorder (4)

A

Arthralgia

Disc disorders

Degenerative joint disease

Subluxation

310
Q

Signs/symptoms of headache attributed to TMD (7)

A

Headache in temporal area modified by jaw movement, function or parafunction

Familiar headache in temple area on palpation of temporalis muscles or movement tests

A diagnosis of pain related TMD must also be present

Ache in temple area

Aggravated with jaw movement, function, parafunction

Pain on movement testing

Pain on palpation of temporalis muscle

311
Q

Masticatory muscles disorders (3)

A

Local myalgia - pain specifically over site of problem

Myofascial pain - referred pain but in boundaries of muscles

Myofascial pain with referral - beyond boundary of muscles, presence of trigger points

312
Q

Masticatory muscles disorders are associated with (3)

A

Painful guarded muscles of mastication

Emotional tension

Parafunctional activity

313
Q

Signs/symptoms of masticatory muscle disorders (5)

A

Pain in masticatory muscle modified by jaw movement, function or parafunction

Familiar pain in muscles on palpation or movement

Pulling/tight/ache sensation

Pain with jaw activity

Tenderness on palpation

314
Q

Signs/symptoms of TMJ arthralgia (2)

A

Pain in TMJ modified by jaw movement, function, parafunction

Familiar pain in TMJ on palpation or movement tests

315
Q

What is disc deplacement with reduction and its signs/symptoms

A

The disc position is no longer maintained on the condyle throughout the range of motion

TMJ noises -clicking, popping, snapping

Deviation

Pain

Locking

316
Q

What is disc displacement without reduction and its signs/symptoms

A

Progression of disc displacement with reduction, disc no longer relocates, folds in front of the condyle

Acute - closed lock, limited opening interfere with ability to eat, maximum passive assisted opening, limited contralateral excursion, ipsilateral deviation with opening, pain

Chronic - joint can become stretched to allow nearly full ROM

317
Q

Signs/symptoms of degenerative joint disorder (5)

A

TMJ noises

TMJ crepitus

Familiar pain in TMJ on palpation or movement tests

Tenderness on palpation

OPT - joint space narrowing, osteophytes, subchondral sclerosis, subchondral cysts

318
Q

What is hypermobility and subluxation and Signs/symptoms of it

A

Condyle displaces beyond the eminence and locks open

TMJ clicking, catching, locking

Lock resolves with specific maneuver

Excession mouth opening

Open locking

Familiar pain in TMJ on palpation and movement tests

319
Q

Aetiology of oral precancer/cancer (7)

A

Multifactorial

Polymorphisms in genes involved in metabolism of carcinogens

Inherited cancer syndromes - Li Fraumeni, Fanconi anaemia

Environmental - Tobacco, Alcohol, Sunlight, Infections, Diet and nutrition

Oncogenes

Tumour supressor geens

Viral component

320
Q

What is leukoplakia

A

White patch that cannot be rubbed off and cannot be characterised clinically or histologically as any other disease

Is not associated with any physical or chemical causative agent except the use of tobacco

321
Q

Epidemiology of leukoplakia (4)

A

No good registration schemes

Precancer

Prevalence from 0.9-26.9%

UK prevalence = 2.8%

322
Q

Features of homogenous leukoplakia (2)

A

Flat and plaque like uniformly white

Related to hyperkeratosis

323
Q

What is this lesion

A

Homogenous leukoplakia

324
Q

Feature of Non homogenous leukoplakia (4)

A

Variation in colour or texture

Speckled

Exophytic nodular

Verruciform - thickened with carpet like surface

325
Q

What is this lesion

A
326
Q

Indications of leukoplakia malignancy potential (5)

A

Site - high risk (lateral margins of tongue, floor of mouth, retromolar, soft palate, fauces), low risk (gingiva, buccal mucosa, labial mucosa, hard palate)

Colour - if red area seen within white, pay close attention

Texture

Presence of candida

Degree of dysplasia

327
Q

What is erythroplakia

A

A red patch on oral mucosa which cannot be characterised clinically or histologically as due to any other condition

Less prevalence than leukoplakia but higher risk of malignancy

328
Q

What is epithelial dysplasia

A

Collective term used to embrace a number of individual atypical features

Graded mild, moderate, severe

Premalignant state with increased risk of cancer development

329
Q

Epithelial dysplasia architectural features (3)

A

Irregular epithelial stratification

Loss of basal cell polarity

Drop shaped rete processes

330
Q

Epithelial dysplasia cytological features (5)

A

Increased numbers of mitotic figures

Cellular and nuclear pleomorphism

Nuclear hyperchromatism

Individual cell keratinisation

Loss of intercellular adherence

331
Q

Changes in mild dysplasia

A

Architecture - Changes in lower third

Cytology - Mild atypia

332
Q

Changes in moderate dysplasia

A

Architecture - Changes in middle third

Cytology - Moderate atypia

333
Q

Changes in severe dysplasia

A

Architecture - changes in the upper third

Cytology - Severe atypia and numerous mitoses, abnormally high

334
Q

What is this lesion

A

Mild dysplasia

335
Q

What is this lesion

A

Moderate dysplasia

336
Q

What is this lesion

A

Severe dysplasia

337
Q

Potential malignant conditions (4)

A

Chronic hyperplastic candidosis

Actinic Keratosis

Submucous fibrosis

Lichen planus

338
Q

What is this lesion

A

Chronic hyperplastic candidosis

339
Q

Features of submucous fibrosis (3)

A

Seen in indians and others asian

Associated with areca nut use (paan)

Mechanism unknown

340
Q

What is this lesion

A

Submucous fibrosis

341
Q

Symptoms of oral cancer (5)

A

None

Soreness/irritation

Paraesthesia/anaesthesia

Disruption of function

Dysphagia

342
Q

Signs of oral cancer (8)

A

Persistent ulcer

Persistent white, red, mixed patch

Exophytic mass

Fixation of tissue

Induration

Sensory/motor deficit

Tooth movement/mobility

Lymph node enlargement/fixation

343
Q

How to diagnose oral cancer

A

Incisional biopsy

344
Q

Types of oral cancer (4)

A

Squamous cell carcinoma

Verrucous carcinoma

Basaloid

Spindle cell

345
Q

What are the different grades that can be used to describe cancers (3)

A

Well differentiated - resembles cell of origin, expresses keratins

Moderately differentiated - resembles cell of origin, may produce some keratin

Poorly differentiated - may not resemble cell of origin, no keratin, central necrosis

346
Q

Features to look for when staging cancer (5)

A

TMN

Overall tumour size

Invasion into muscle

Involvement of nerves/blood vessels

Invasion into bone

347
Q

Signs and symptoms of lymph node metastasis (3)

A

Painless enlargement

Rock hard mass

Fixation - indication tumour has spread from node into surrounding tissues

348
Q

Conservative treatment of OACs (5)

A

Many undetected - heal spontaneously

Instructions - no nose blowing, OHI

Antibiotics - broad spectrum

Splints - rarely used

Decongestants - stop them sneezing or blowing nose

349
Q

Active treatment of OACs (4)

A

Suturing

Packing

Antibiotics

Decongestants

350
Q

What is an oral antral fistula

A

Fistula is an abnormal connection or passageway between two epithelium lined organs or vessels that normall do not connect - OAC may heal forming OAF

351
Q

OAF symptoms (7)

A

Purulent discharge

Bad taste

Liquid discharge through nose

Air escape

Episodic sinusitis

Demonstration of communication

Radiographic evidence

352
Q

Management of OAFs

A

Buccal advancement flap or palatal rotation flap

Post op care - analgesics, amoxicillin 250mg TDS for 5 days

Ephedrine hydrochloride 0.5%, good OH, No nose blowing for 4 weeks, no singing

353
Q

How to manage displaced foreign objects in the antrum

A

Retrieve object - suction, irrigation, radiograph

Refer

354
Q

Chronic sinusitis symptoms and treatment

A

Bacterial or viral

Symptoms - can mimic toothache, nasal discharge, pressure, pain when bending over/lying down

Radiograph - cloudiness around sinus

Treatment - bacterial (antibiotics, decongestants), chronic (antral wash out, nasal surgery

355
Q

What is trigeminal neuralgia

A

Sudden, unlateral, severe, brief stabbing, recurrent pain distributed in one or more branches of the fifth cranial nerve

356
Q

Presentation of trigeminal neuralgia (7)

A

Unilateral, sharp shooting pain

Triggered by movement

Paroxysms

Remission

Depression

Suicidal

Isolated

357
Q

Pathophysiology of trigeminal neuralgia (5)

A

Local demyelination of the trigeminal root but not fully understood

Demyelination could be caused when the cerebellar artery sits on top of trigmeical nerve (idiopathic neuralgia - not always)

Alternatively a tumour could be sat on the nerve

Action potential from one nerve fibre jumps to another nerve fibre

Therefore pain signal from one is spread to others

358
Q

Management of trigeminal neuralgia

A

Sodium channel blockers - carbamazepine 2 x daily, oxcarbazepine, lamotrigine 25mg 1x daily 2 weeks, then 2 x daily 2 weeks

Gabapentin

Baclofen

Valproate

Phenytoin

Microvascular decompression - taking blood vessels from nerve and placement sponge

359
Q

Indications for orthognathic surgery (4)

A

Psychosocial - embarrassment (patients unhappy with appearance)

Function - eating, speech, obstructive sleep apnea

Non growing adult

Severe on IOTN

360
Q

Contraindications for orthgnathic surgery (6)

A

BMI >35

TMJ - small condyles as resorption can occur after surgery

Blood dysrasias

Mental health issues

Bone disorders - osteoporosis

Medications - bisphosphonates

361
Q

Sequence of orthognathic surgery

A

Joint clinics and facial planning

Extractions

Presurgical orthodontics

Surgery

Postsurgical orthodontics

362
Q

What is the purpose of staging in cancer

A

Accurately define the extent of the primary cancer, including the structures it invades into as well as those structures that might be included in resection if surgery is performed

Allows you to select most appropriate treatment

Allows you to predict prognosis

363
Q

TMN - T classification

A

T0 = no evidence of primary tumour

T1 = tumour smaller than or equal to 2cm

T2 = tumour bigger than 2cm but smaller than 4cm

T3 = tumour bigger than 4cm

T4 = invades deep structures

364
Q

TMN - N classification

A

N0 = no lymph node metastases

N1 = single ipsilateral node less than 3cm, ENE negative

N2a = single ipsilateral node, between 3 and 6cm, ENE negative

N2b = multiple ipsilateral nodes less than 6cm, ENE negative

N2c = contralateral/bilateral node(s), ENE negative

N3a = any node more than 6cm, ENE negative

N3b = any node that is ENE positive

365
Q

TMN - M classification

A

M0 = no distant metastases

M1 = distant metastases present

366
Q

The role of a pathologist

A

Prior to treatment - establish diagnosis, staging grading

During treatment - provision of froxen diagnosis to determine completeness of excision

After treatment - determine completeness of excision, report on factors important to prognosis and further planning

367
Q

Post op care/complications faced by OMFS oncology patient (7)

A

Tracheostomy

FOM surgery

Flap

Artificial feeding

Changes in mobility

Communication

Managing pain

368
Q

What is anaplastology

A

Restoration of absent parts of the body through artifcial means

369
Q

What is melanin produced by

A

Melanocytes - not usually seen as they are clear

370
Q

What type of cells are melanocytes

A

Dendritic because the branches of the cell distributes melanin

371
Q

Where are melanocytes found

A

Basal third of epithelium

372
Q

What colour are melanocytes

A

Black/brown tinge to basal cells due to the melanin

373
Q

How is melanin transferred

A

Transferred to adjacent keratinocytes via membrane bound organelles called melanosomes

374
Q

What is a melanoma

A

Increased number/abnormal melanocytes

375
Q

How does a haemosiderin work

A

Breakdown product from RBCs, where iron is stored

Causes brown colour

376
Q

How does amalgam cause pigmentation

A

Heavy metals may leach into mucosa from dental restoration and crowns

377
Q

What are chromogenic bacteria

A

Bacteria that produce pigment

Mainly aspergillus, actinomyces

Often seen in hairy tongue

Bacterial enzymes act on iron compounds in saliva

378
Q

Types of exogenous oral pigmented lesions (4)

A

Amalgam tattoo

Foreign body tattoo

Heavy metal

Black hairy tongue

379
Q

Features of amalgam tattoo (3)

A

How - Tattoo adjacent to an amalgam restoration extracted, amalgam deposits fall into extraction socket or retrograde filling for an apicoectomy is done using amalgam

Histologically - amalgam follows the collagen fibres and goes around the blood vessels by staining them black

Radiographically - may show radioopacities where tattoo is, if it doesn’t show up or is slightly darker than it should be = refer

380
Q

Features and treatment of black hairy tongue (6)

A

Affects posterior dorsal tongue

Decrease in normal desquamation process

Elongated filiform papillae - black, brown, white

Discolouration - caused by chromogenic bacteria, chlorhexidine, foods, smoking

Doesn’t need a biopsy because it is a clinical diagnosis

Treatment - advise a tongue scraper to thin the mucosa

381
Q

Types of Endogenous oral pigmented lesions

A

Developmental - Physiological, Peutz Jeghers syndrome, McCune Albright, Haemochromatosis, Pigmented naevus

Acquired - addisons disease, drug induced, post inflammatory, smokers melanosis, melanotic macule

Neoplastic - malginant melanoma, kaposi sarcoma

382
Q

Features of Peutz Jeghers syndrome (4)

A

Genetic disorder - autosomal dominant

Pigmented mucocutaneous macules, GI polyps, usually small intestine with normal increased risk of malignant change associated with polyps

Melanotic spots characteristically small and multiple

Very obvious around the lips

383
Q

Features of McCune Albright (5)

A

Autosomal dominant

Mutations in GNAS gene

Polyostotic fibrous dyplasia

Endocrine abnormalities

Cafe aux lait pigmentation, commonly around lips

384
Q

Histological features of McCune Albright (2)

A

Increase in amount of melanin

All freckles look same - histology isn’t much help so it is a clinical diagnosis

385
Q

Features of Haemochromatosis (6)

A

Genetic disorder - autosomal recessive

Accelerated rate of intestinal iron absorption

Raised serum ferritin and transferrin saturation

Accumulation of iron (haemosiderin)

Leads to bronze skin pigmentation, liver cirrhosis, diabetes mellitus

Occurs later in women - menstruation stops so iron builds up

386
Q

Features of pigmented naevus (2)

A

Melanin is also syntehsised by naevus cells which are derived from the neural crest

Found in skin and mucosa

387
Q

Histological features of different types of pigmented naevus (3)

A

Junctional epithelium - confined to the epithelium, brown circles

Intradermal/mucosa - confined to the dermis/lamina propria

Compound - some at surface, some in laminar tissue

388
Q

How Addisons disease leads to oral pigmentation

A

Destruction of entire adrenal cortex (autoimmune?)

Lack of adrenocortical hormone = production of adrenocorticotropic hormone by anterior pirtuitary gland

ACTH

389
Q

How do drugs induce acquired oral pigmentation (3)

A

Increased production of melanin

Deposition of iron after damage to mucosal vessels

Deposition of heavy metal in tissues (exogenous)

390
Q

Drugs that can cause oral pigmentation lesions

A

Antimalarials

Quinindine

Zidovudine

Tetracycline

Minocycline

Chlorpromazine

Oral contraceptives

Clofazimine

Ketoconazole

Amiodarone

Busulfan

Doxorubicin

Bleomycin

Cyclophosphamide

391
Q

Features of post inflammatory cause of oral pigmentation (3)

A

Melanin can drop into the lamina propria

Patchy erythema

Lichen planus causes damage to basal cells

392
Q

Features of smokers melanosis (3)

A

Most commonly buccal mucosa and palate

May also have hairy tongue or tooth staining

No significant basal cell loss

393
Q

What is a malignant melanoma

A

Proliferation of malignant melanocytes along the junction between the epithelial and connective tissues, as well as within the connective tissue

394
Q

Key features of malignant melanoma (4)

A

Asymptomatic

Slow growing brown/black patch with asymmetry and irregular borders vs rapidly enlarging mass associated with ulceration, bleeding, pain and bone destruction

Some non pigmented (amelanotic)

Aggressive and often fatal disease

395
Q

Treatment for malignant melanoma

A

Radical surgical excision with clear margins

396
Q

Histological features of malignant melanoma

A

Melanocytes invade into the connective tissue

397
Q

Features of Kaposi sarcoma (7)

A

Malignant tumour

Associated with immunosuppression

Hallmark of AIDS

Caused by HHV 8

Black/purple lesions orally

Haemosiderin gives brown colour to these lesions

Vascularity gives red/blue colour

398
Q

Treatment for Kaposi sarcoma

A

Excision +/- chemo/radiotherapy

399
Q

What is this lesion

A

Malignant melanoma

400
Q

What is this lesion

A

Hairy tongue

401
Q

What is this lesion

A

Amalgam tattoo

402
Q

What is this lesion

A

Peutz Jeghers syndrome

403
Q

What is this lesion

A

McCune Albright

404
Q

What is this lesion

A

Kaposi sarcoma

405
Q

What is a cyst

A

Pathological cavity with fluid, semi fluid or gaseous contents, which is not created by the accumulation of pus

If formed by pus, it would be an abscess

406
Q

Where do cysts come from

A

Enamel organ develops from dental lamina

PDL contains epithelial remnants of Hertwigs root sheath which is scattered throughout it and especially concentrated at apex

Stimulus for rest cells of Malassez to develop into radicular cysts

407
Q

What is needed to create a cyst (3)

A

Source of epithelium - remnants of odontogenic epithelium (Hertwigs rooth sheath = radicular cysts, Reduced enamel epithelium = dentigerous cysts, Remnants of dental lamina = keratocysts, gingival cysts, ameloblastoma)

Stimulus for proliferation - inflammation (apical granuloma = radicular cyst, periodontitis = lateral periodontal cyst, pericoronitis = paradental cyst), developmental (eruptive force/hydrostatic pressure = dentigerous cyst, epithelial proliferation/tumour = keratocyst)

Pathogenesis - osmosis and hydrostatic pressure, proliferation of the lining, bone resorption

408
Q

How osmosis and hydrostatic pressure causes cysts (3)

A

Inflammation, cell shedding and cell death results in increased osmotic presure

Water is drawn in by osmosi, increasing the hydrostatic pressure, resulting in uncentric expansion

Occurs in radicular and dentigerous cysts

409
Q

How bone resorption causes a cyst

A

IL1 and IL6, prostaglandins, endotoxins

Stimulation and activation of osteoclasts and inhibition of osteoblasts

Non vital tooth containing bacteria within root canal system

Bacteria produce endotoxins

Stimulates inflammatory response and specific immune response

Leading to response dominated by helper T cells

Resulting in production of a number of cytokines

Also activation of fibroblast cells which further release growth factors such as keratinocyte growth factor and fibroblasts growth factor

Act upon epithelium stimulating it to proliferate

410
Q

Features of a radicular cyst (5)

A

Odontogenic

Inflammatory

Always associated with a non vital tooth

Spread of inflammation to the periapical tissues gives stimulus for the developmemt of the cyst

Location depends on where the opening of the root canal is

411
Q

Features of a residual cyst (4)

A

Odontogenic

Inflammatory

Type of radicular cyst

Removal of tooth with radicular cyst but cyst left behind

412
Q

Types radicular cysts (3)

A

Apical

Lateral

Residual

413
Q

Radiographical features of a radicular cyst

A

Well defined radiolucency

Not corticated

External resorption of the root may occur

414
Q

Pathogenesis of radicular cyst (8)

A

Caries

Pulp necrosis

Extension of inflammation into periapex

Periapical periodontitis

Chronic periapical periodontitis

Periapical granuloma

Proliferating odontogenic epithelium

Cyst

415
Q

Histological features of radicular cyst (4)

A

Irregular lining of non keratinised stratified squamous epithelium with thick and thin areas

Inflammatory cells within connective tissue closely associated with lining indicating an inflammatory cyst

Wall of cyst comprises of fibrous connective tissue and inflammatory cells (lymphocytes, plasma cells, neutrophils, macrophages)

Plasma cells have fried egg appearance with nucleus to one side

416
Q

Features of a paradental cyst (4)

A

Arises on lateral aspect of a tooth as a result of inflammation in a periodontal pocket or pericoronitis

Associated with partially erupted tooth

Arises from pocket epithelium

Histology similar to radicular cyst

417
Q

What is a follicular cyst

A

Cysts surrounding the crown of an erupted tooth and arise from reduced enamel epithelium

418
Q

Types of follicular cysts

A

Dentigerous - associated with impacted tooth

Eruption - associated with an erupting tooth

419
Q

Histological features of a follicular cyst (4)

A

Cyst attaches to the tooth at ACJ

Lining is bilayer of cuboidal epithelium as it arises from reduced epithelium

Sometimes epithelium is more proliferative and so thin non keratinised stratified squamous epithelium seen

Wall made up of fibrous connective tissue with no inflammatory cells as it is developmental and not inflammatory

420
Q

What is an odontogenic keratocyst

A

Cyst arising in tooth bearing area and characterised by thin lining of parakeratinised epithelium

Arises from dental lamina or its remnants

421
Q

Features of an odontogenic keratocyst (5)

A

Very large

Tend to present at angle of mandible as dental lamina and its remnants are scattered predominantly in posterior part of mandible

May replace tooth

Grows and actively proliferates in jaw therefore does not have a balloon like unicentric expansion shape, sometimes multilocular appearance

Sometimes anterior posterior expansion

422
Q

Histological features of odontogenic keratocyst (7)

A

Parakeratanised lining

Thin epithelium of 5-10 cells thick

Thin layer of keratin but retaining its nuclei on its surface

Palisaded nucelar feature

Flat interaction with underlying connective tissue

Surface epithelium can sometimes become bumpy/coorugated

No inflammatory cells

423
Q

Why do odontogenic keratocysts recur (2)

A

Fragility of lining - thin, easy to leave behind bits of epithelium during nucleation

Daughter cysts - produces keratinised balls of epithelium into the wall of cyst, if lining removed, balls of epithelium would be left behind to develop into daughter cysts

424
Q

Faetures of Gorlin Goltz syndrome (6)

A

Inherit abnormal copy of PTCH gene on chromosome 9

Multiple and recurrent odontogenic keratocysts

Basal cell carcinomas of skin

Frontal bossing

Skeletal abnormalities

Cranial abnormalities

425
Q

Features of a lateral periodontal cyst (4)

A

Occurs on lateral aspect between roots of vital teeth

Occasionally multilocular and call botyroid odontogenic cyst

Radiographic appearance will appear well definied non corticated lesion between roots of vital teeth

Histology shows no inflammation within wall, localised thickening of wall is common

426
Q

Features of gingival cysts in infants (4)

A

Arises from dental lamina in the alveolar mucosa of infants

Lined by thin parakeratinised epithelium

Present for very short time after birth before disappearing

Similar to later periodontal cyst but further up and in soft tissues

427
Q

Features of gingival cysts in adults (3)

A

Arises from dental lamina rests in attached gingiva

Believed that gingival cysts in adult are same as lateral periodontal cysts but location differs

Histologically lined with thin non keratinised squamous epithelium with some localised thickening of lining similar to lateral periodontal cyst

428
Q

Features of glandular odontogenic cyst (5)

A

Very rare

Cyst characterised by cuboidal or columnar epithelium with mucous production

Forms duct like or glandular structures

Can be very aggressive and destructive with high recurrence rate like odontogenic keratocyst

Histology - lining has holes in it with mucous cells and gland like structures

429
Q

Features of calcifying odontogenic cyst (4)

A

Epidemiology - 10-30 y/o

Radiograph - Well defined radiolucency, Non corticated, May have calcifications

Histology - Epithelium undergoes ghost cell change which can become calcified

Cyst lined by ameloblastoma like epithelium with ghost cells and dentine in the wall, may be solid

430
Q

Features of nasopalatine duct cyst (3)

A

Arise in nasopalatine canal from epithelial residues of the nasopalatine duct

Occurs in midline of anterior palate

Remnants of epithelium which didn’t undergo apoptosis after the fusion of the medial and lateral palatine processes gives the basis for the formation of the nasopalatine duct cyst

431
Q

Radiographic appearance of nasopalatine duct cyst

A

Oval/heart shaped, well defined, non corticated radiolucency in midline between upper incisors

If lamina dura of central incisors is continuous with radiolucency of cyst = radicular cyst

432
Q

Histological features of nasopalatine cysts (2)

A

Lined with respiratory epithelium (ciliated pseudostraitified squamous epithelium with goblet cells) or stratified squamous epithelium

Look for artery and nerve in wall of cyst

433
Q

Cyst like lesions

A

Solitary boen cyst - incidental findings, when surgically explored drop into a cavity in jaw which contains air, no lining, heal after curettage, no known cause

Stafne bone cavity - not really a cyst, radiographic appearance similar to a cyst, indentation in lingual side of mandible which sits part of the submandibular gland

434
Q

What is this lesion

A

Radicular cyst

435
Q

What is this lesion

A

Dentigerous cyst

436
Q

What is this lesion

A

Odontogenic keratocyst

437
Q

What is this lesion

A

Nasopalatine duct cyst

438
Q

Features of a nasolabial cyst

A

Arises in soft tissue overlying alveolar process at base of nostril, deep to nasolabial fold

Arises from remnants from formation of nasolacrimal duct and usually lined by pseudostratified columnar epithelium

439
Q

General approach for cyst management (4)

A

Enucleation - removal in entirety without cutting

Curettage - removal of tissue by scraping or scooping

Resection - removal of part of an organ, takes pathology and margin of normal tissue

Marsupialisation - creation of a pouch by suturing cyst lining to external surface

440
Q

Radicular cyst management options (4)

A

RCT

Extract causative tooth

Extract causative tooth +/- enucleate cyst

Rarely marsupialise +/- further therapy

Apicectomy - indicated if persistent symptoms in non vital tooth, Re-RCT infeasible, not just cysts, contraindicated if previously tried, poor OH, molars, active caries, severe bleeding disorder, unrestorable, endocarditis risk

441
Q

Management of dentigerous cysts

A

Enucleate along with removing unerupted tooth

Eruption cyst requires no treatment

442
Q

Management of Mucous extravasation

A

Blunt dissection/excision

Difficulty with removing - housed in soft tissue, scarring/fibrosis, not epithelially lined

443
Q

How to remove keratocyst

A

Fixate and enucleate

444
Q

How many millimetres of root are generally removed during apicectomy

A

3mm

445
Q

What angle should you perform apicoectomy at

A

90

446
Q

What is the risk of using fixative to remove a keratocyst

A

ID nerve damage

447
Q

Management of eruption cyst

A

Conservative advice and review

448
Q

Clinical signs Rheumatoid arthritis (11)

A

Insidious onset

Pain and stiffness of small joints

Fatigue and malaise

Anaemia

Weight loss

Muscle weakness and wasting

Neurological effects

Lymphadenopathy

Lung problems - pleural effusion and pleural nodules

Sjogrens syndrome

TMJ damage

449
Q

How to diagnose Rheumatoid arthritis

A

Clinical

Radiographic changes

Anaemia

Raised ESR, CRP

Anti CCP positive

Rheumatoid factor positive

ANA positive

450
Q

Management of Rheumatoid Arthritis (2)

A

General - Education, Exercise, Physio, Surgery, Dietary advice

Specific - DMARDs (methotrexate, gold, penicillamine, hydroxychloroquine, cyclosporin), Corticosteroids, Biological agents (adalimumab, etanercept, infliximab, rituximab), NSAIDs, COX2 inhibitors

451
Q

Oral effect of methotrexate

A

Oral ulceration

452
Q

Oral effect of gold

A

Lichenoid reactions

453
Q

Oral effect of Penicillamine (3)

A

Loss of tatse perception

Lichenoid reactions

Severe oral ulceration

454
Q

Oral effect of hydroxychloroquine

A

Lichenoid reactions

455
Q

Oral effect of Cyclosporin

A

Gingival hyperplasia

456
Q

Oral effect of Adalimumab

A

TB, Oral candidosis, erythema, multiforme, lichenoid reactions, Oral SCC

457
Q

Oral effect of NSAIDs

A

Stomatitis

Erythema multiforme

Gastrointestinal bleeding - candidosis, burning tongue, depapillated tongue

458
Q

Orofacial aspects of Rheumatoid arthritis (5)

A

Access

Atlantoaxial joint dislocation

Impaired manual dexterity

Secondary Sjogrens syndrome

Feltys syndrome

459
Q

Aetiology of Lupus erythematosus (4)

A

Genetic predisposition

Environmental trigger

T cell dysregulation of B cell activity

Possible defect in clearance of apoptotic cells

460
Q

Two forms of Lupus erythematosus

A

Discoid Lupus erythematosus

Systemic Lupus Erythematosus

461
Q

Features of DLE (3)

A

Affecst skin and oral mucosa - lichen planus on palate, scaly erythematous patches, atrophic hypopigmented areas, occur on sun exposed areas, may be premalignant

More in females than males

Peak incidence = 40 years

462
Q

How to diagnose DLE (3)

A

Clinical appearance

Biopsy

Immunology - ANA, dsDNA

463
Q

Management of DLE

A

Treat as lichen planus

464
Q

Features of SLE (3)

A

Onset at 30 y/o

More in females

Systemic - malar rash, polyarthritis, photosensitivity, oral lesions (uni or bilateral white patches with centre of erythema or ulceration, may involve palate, may be extensive)

465
Q

How to diagnose SLE (2)

A

Clinical

Immunological

466
Q

Pharmacological management of SLE (4)

A

NSAIDs

Hydroxychloroquine

Corticosteroids

Cytotoxic drugs

467
Q

What is systemic sclerosis

A

Autoimmune disorder

Dense collagen is deposited in the tissues of the body

468
Q

Features of systemic sclerosis (6)

A

Sympathetic nerves supplying the blood vessels cause the blood vessels to constrict

Loss of colours of fingers or red and painful fingers

While fingers are ischaemic, ulcers can develop

Sausage like fingers

May lose fingernails and ultimately have fingers amputated

Mephadpine used to treat it

469
Q

Types of systemic sclerosis (3)

A

Localised cutaneous - limited to skin on face, hands, feet, development of pulmonary arterial hypertension after 10-20 years

Diffuse cutaneous - more extensive, may progress to visceral organs, death most often from pulmonary, heart and kidney involvement

CREST syndrome - calcinosis, Raynauds phenomenon, esophageal dystfunction, sclerodactyly, telangiectasia

470
Q

Orofacial manifestations of systemic sclerosis (14)

A

Facial skin rigidity

Sharp nose

Thinning of lips

Loss of facial wrinkles

Microstomia

Hypomobile tongue

Dysphagia and xerostomia

PDL widening

Pseudoankylosis of TMJ

Speech

Bite affected

Eating

Deteriorating quality of life

471
Q

How to diagnose systemic sclerosis (5)

A

Clinical

Skin biopsy

Scl - 70 autoantibodies

High resolution CT of chest

PDL widening

472
Q

Management of systemic sclerosis (5)

A

Nifedipine

D-penicillamine

Iloprost infusions

Sildenafil

DMARDs

473
Q

Features of Sjogrens syndrome (4)

A

Autoimmune exocrinopathy (affects exocrine glands)

Primary and secondary (RA/SLE)

Focal lymphocytic infiltration of salivary and lacrimal glands

Mouth must be dry for at least 3 months

474
Q

Aetiology of Sjogrens syndrome

A

Genetic predisposition

Viral agents - Herpes virus, Hep C, Retroviruses

475
Q

Pathogenesis of Sjogrens syndrome (5)

A

Lymphocytic infiltration of exocrine glands

Hypertrophy of ductal epithelium

Formation of epimyoepithelial islands

Acinar atrophy and fibrosis

Probable hyperactivity of B cells

476
Q

Subjective symptoms of xerostomia in patients with Sjogrens syndrome (10)

A

Difficulty swallowing/chewing dry food

Sensitivity to spicy food

Altered salty bitter metallic taste

Burning mucosa

Lack or diminshed taste

Salivary gland swelling/pain

Cough

Voice disturbance

Nocturnal discomfort

Increased risk of thrush and decay

477
Q

Oral signs of Sjogrens syndrome (4)

A

Oral mucosa - dry, atrophic, wrinkled, ulcerated, increased debris

Tongue - dry, red, lobulated, loss of papilla

Teeth - increased caries

Salivary glands - firm on palpation if swollen

478
Q

Management of Sjogrens syndrome

A

Palliative - increase lubrication, maintain oral/dental health, review candida status

Therapeutic - pilocarpine, immunodulating agents

479
Q

Xerostomia vs Hyposalivation

A

Xerostomia is symptom of oral dryness - may exist with or without hyposalivation

Hyposalivation is an actual decrease in saliva flow rate

480
Q

Function of saliva (8)

A

Lubricant effect

Physical cleanser

Caries control

Prevent demineralisation

Pellicle formation

Antimicrobial

Taste

Digestion of carbohydrates

481
Q

Effects of long standing xerostomia (10)

A

Difficulties in oral function and denture wear

Increase in frequency of caries

Acute gingivitis

Dysarthria

Dysphagia

Taste disturbances

Increase susceptibility to oral candidosis

Burning tomgue/depapillation of tongue

Dry, sore cracked lips

Salivary gland enlargement

482
Q

Factors associated with hyposalivation/xerostomia (6)

A

Anxiety/depression

Dehydration

Drugs

Radiotherapy

Diabetes

Over 65 y/o

483
Q

Drug related xerostomia causes

A

Tricyclics

SSRIs

Antihistamines

Diuretics

Sympathomimetics

Anticholinergic

Antipsychotics

Antiparkinsonian

Sedatives

484
Q

Other causes of xerostomia/hyposalivation

A

Radiation induced salivary dysfunction

Chemotherapy induced salivary dysfunction

Autoimmune

Infections - HIV, Hep C, CMV, EBV

Rare - amyloidosis, haemochromatosis, Wegners disease, Salivary gland agenesis

485
Q

Special investigations for xerostomia/hyposalivation

A

Clinical - Sialometry, Schirmers test, Rose bengal staining, Labial gland biopsy

Radiological - USS, Sialography, salivary scintigraphy, PET scan, MRI, CT

Lab based - immunology, haematology, SACE, liver function, thyroid function, cryoglobulins

486
Q

Histopathological features of Sjogrens syndrome (5)

A

Acinar loss

Duct dilation

Periductal fibrosis

Focal lymphocytic infiltrate

Focal aggregate of at least 50 lymphocytes

487
Q

Treatment of xerostomia/hyposalivation (8)

A

Directed at underlying cause

Prevention is key due to lack of efficacy of saliva replacement therapy

Assess patients before radio/chemotherapy

Manage xerostomia early

Prevent dental complications

MDT approach

Stimulation of saliva production

Use saliva substitutes

488
Q

Prevention strategy for dental caries in xerostomia (7)

A

Patient education

Diet and nutrition counselling

Hygiene control

Fluoride

Microbial control

Rehydration therapy

Dental - 3 monthly visits, FS, GIC

489
Q

Management of dry mouth (6)

A

Oral moisturisers - saline, water

Gustatory and mechanical stimulation of salivation - acidic stimulation, sugarless gum, lozenges, acupuncture

Special toothpaste/mw

Saliva substitutes

Lip creams and ointments

Systemic therapy

490
Q

Oral manifestations of HIV group 1 lesions (5)

A

Candidosis - erythematous, pseudomembranous, treatment = topical (miconazole), systemic (fluconazole)

Hairy leukoplakia - lesions bilateral of tongue, corrugated, not premalignant, caused by EBV, treatment = no treatment, may regress with acyclovir but returns after

HIV associated periodontal disease - manage by removal of necrotic bone, debridement, antibiotics (metronidazole), OHI

Kaposis sarcoma - non blanching nodules, management = radio, chemo, surgical excision

Non Hodgkins lymphoma - management = radio, chemo

491
Q

Oral manifestation of HIV group 2 lesions (4)

A

Atypical oropharyngeal ulceration

Idiopathic thrombocytopenia purpura

Salivary gland disorder - dry mouth, decrease in salivary flow rate, swelling of SG

Viral infections other than EBV - cytomegalovirus (oral ulcers), herpes simplex (secondary herpes), Human papillomavirus (multiple warts), Herpes zoster (severe shingles)

492
Q

Oral manifestation of HIV group 3 lesions (4)

A

Oral bacterial infections other than periodontal disease

Fungal infections other than candidosis

Melanotic hyperpigmentation

Neurological disturbances - trigeminal neuralgia, facial palsy

493
Q

Management of HIV

A

Systemic - Highly active antiretroviral therapy, Prophylactic treatment for opportunistic infections and tumours

Dental - GDP

Oral manifestations - treatment as per lesion requirement

494
Q

Aetiology of CLP

A

Genetic

Environmental - anticonvulsant drugs, nutritional deficiency, anaemia, alcohol, low socioeconomic status

Genetic predisposition triggered by environmental factors

495
Q

How to diagnose CLP

A

Antenatal scan (20 wks)

496
Q

Diagnostic features of submucous cleft palate (3)

A

Notch on palatal shelf

Bifid uvula

Blue translucent zone - all muscles that should be transverse are placed oblique

497
Q

Syndromes associated with cleft palate (3)

A

Van de Woude - autosomal dominant, lip pits, cleft palate, linked with cardiac anomalies, hypodontia

Pierre robin sequence - cleft palate, glossoptosis, mandibular retrognathia, stickler syndromes

Foetal alcohol syndrome - significant developmental delay, failure to thrive and learning difficulties

498
Q

Features of ameloblastoma

A

Benign

Locally destructive

Clinical - often asymptomatic, buccolingual expansion, root resorption or displacement

Histological - columnar ameloblast like cells at periphery, stellate reticulum like area in centre, epithelium resembles enamel organ, cysts form in stellate reticulum like areas

499
Q

Management of ameloblastoma (2)

A

Conventional - excision with margins, reconstruction

True unicystic - enucleation, careful follow up

500
Q

Features of adenomatoid odontogenic tumour

A

Benign, does not recur

Probably hamartoma

Radiolucency around crown of tooth

DD = dentigerous cyst

Histological - epithelial cells forming sheets and duct like structures, calcifications common

501
Q

Treatment for adenomatoid odontogenic tumour

A

Enucleation

502
Q

Features of calcifying epithelial odontogenic tumour aka Pingbord tumour

A

Benign but locally destructive

Radiolucency with speckled calcification

Histological - enamel matrix material which may calcify, cuboidal cells with prickles, composed of pleomorphic epithelium with calcifications, dentinoid and amyloid

503
Q

Features of ameloblastic fibroma

A

Benign

Well defined radiolucency - 80% associated with unerupted tooth

Histological - branching cords and islands of epithelium resembling enamel organ/dental lamina, characteristic fine cellular stroma

504
Q

Features of a dentinogenic ghost cell tumour

A

Benign

Radiolucency, may have calcifications

Histological - epithelium resembling ameloblastoma, ghost cells and dentine, overlap with calcifying odontogenic cyst

505
Q

Features of myxoma/myxofibroma

A

Benign but locally destructive

Clinical - slow growing, painless swelling

Uni or multilocular radiolucency - soap bubble appearance, root displacement or resorption

Histological - triangular/stellate cells in loos myxoid stroma

506
Q

Treatment for myxoma/myxofibroma

A

As for ameloblastoma - excision, reconstruction, enucleation, careful follow up

507
Q

Features of odontogenic fibroma

A

Central and peripheral types

Most often unilocular radiolucency

Histology - mature fibrous tissue, variable amounts of inactive odontogenic epithelium

508
Q

Features of cementoblastoma

A

Benign

Radiopaque lesion attached to tooth root

Histology - sheets of cementum and osteoid in a mosaic pattern, many plump cementoblasts

Resembles osteoblastoma

509
Q

Features of developmental anomalies causing non neoplastic lesions of SG (4)

A

Very rare

May see aplasia (failure to develop/function properly) - associated with other anomalies or syndromes

Heterotopic (non normal tissue mixed in with normal tissue) salivary tissue

Appears corticated and well defined at angle of mandible on radiograph

510
Q

Features of acute parotitis (6)

A

Type of bacterial sialadenitis

Ascending infection - starts in SG in mouth and travels up to parotid

Oral bacteria (S.aureus)

Acute swelling and pain

Pus excudes from ducts

Usually secondary to dry mouth

511
Q

Features of recurrent parotitis in adults (6)

A

Type of bacterial sialadenitis

Recurrent infection

Secondary to dry mouth/xerostomia

Often unilateral

Due to recurrent ascending infections

Secondary to Sjogrens syndrome, drug induced dry mouth, radiation damage

512
Q

Features of recurrent parotitis in children (8)

A

Type of bacterial sialadenitis

May resolve at puberty

Bilateral parotid swellings

No obvious cause or predisposing factors

No pus

Punctate sialectasis

Gradual irreversible destruction of acinar elements

Reduced flow

513
Q

Features of viral sialadenitis (5)

A

Acute bilateral parotid swelling

In children

Very painful, malaise, fever

Self limiting in 10-14 days

May spread to other glands/organs

514
Q

Features of salivary calculi (3)

A

Concentric accumulation of calcium and phosphate salts which deposit around cellular debris or mucous in the salivary ducts or gland

Unilateral

Ask if swelling is associated with meal times

515
Q

Features of radiation sialadenitis

A

Occurs at doses over about 20Gy

High risk of permanent damage over 30Gy

Severe damage at doses of over 50Gy

Serous acini most sensitive

Inflammation and fibrosis of glands

Loss of function

Histological - inflammatory cells scattered around which are not usually present in healthy gums

516
Q

Features of a mucous cyst (7)

A

Lower lip = common site

May also arise on palate, tongue, cheek

Most common in children

Usually extravasation cysts

Painless swellings

Rupture and recur

Types = extravasation or retention

517
Q

Features of a mucous extravasation cyst (6)

A

85% of mucoceles

20-30 yrs

Lower lip

Ruptured duct causing saliva to spill out into connective tissue - cyst lies in mucosa

Lined by fibrous and granulation tissue

Histological - lumen filled with mucous, macrophages filled with mucous, lining of inflamed granulation tissue

518
Q

Features of a mucous retention cyst (6)

A

15% of mucoceles

50-60 yrs

Floor of mouth, buccal mucosa

Due to a blocked duct causing swelling of duct

Lined by duct epithelium

Hardly any inflammatory cells present compared to MEC

Histological - blockage of duct leads to dilation and cyst formation, lumen filled with mucous, cyst wall of fibrous tissue with gland

519
Q

Features of ranula (7)

A

Arise in floor of mouth

Extravasation cyst

Arise from sublingual gland

Painless swelling

Rupture and recur

10-20 y/o

Usually 2-3 cm

520
Q

Features of superficial mucoceles (5)

A

Common sites - palate and buccal mucosa

Extravasation type of cysts

Present like a small subepithelial blister like lesions

Need to differentiate from pemphigoid

Cyst may be raised and may rupture

521
Q

Features of necrotising sialometaplasia (7)

A

Important because it can be mistaken for a malignancy

Presents as indurated (hardened), ulcerated swelling with raised borders

Histological - Squamous metaplasia of salivary duct - islands of squamous epithelium deep in connective tissues, necrosis of acini with ghosts of normal structures

Usually on palate

Often biopsied as malignant

Heals spontaneously in 4-8weeks

Benign inflammatory disease

522
Q

Features of pleomorphic adenomas (benign) (6)

A

Lobulated tumour mass

Lobules are within a capsule

Infiltration of tumour into the capsule may be seen

Epithelium forms strands and islands

Ductal strutcures often seen

Occasional tumours are solid

523
Q

Features of Warthin tumour (6)

A

Irregular cysts

Lined by oncocytic duct epithelium

Stroma composed of lymphoid tissue

Always parotid gland

Bilateral or multifocal

Benign

524
Q

Features of mucoepidermoid carcinoma (7)

A

Mixture of mucous cells and epidermoid

Lesions usually multicystic

High grade lesion may be solid with few mucous cells

Occasional lesions have many clear cells

Parotid most common site

Usually on palate, cheek, retromolar pads

10% metastasise

525
Q

Features of adenoid cystic carcinoma (7)

A

Parotid most common, usually on palate, cheek, sinuses

Highly malignant

Infiltrative tumour - no capsule

Has a characteristic multicystic or cribriform pattern

75% of patients died within 20 years

Metastasis via bloodstream

Infiltrates widely through bone, in blood vessels and along nerves

526
Q

Features of polymorphous adenocarcinoma (5)

A

Well demarcated, lobular outline

Cribriform pattern and washed out nuclei

Only found intraorally - palate, lips, cheek

Infiltrative growth

Bland, monotonous cytology

527
Q

Features of acinic cell carcinoma (4)

A

Microcystic pattern or follicular

About 5% of salivary gland malignancies

Lymphoid tissue and germinal centres are common

Histological - solid, microcystic, papillary cystic, follicular

528
Q

Features of carcinoma in pleomorphic adenoma (5)

A

May appear to typical pleomorphic adenoma

Shows areas of cytological atypia

Some lesions contain other types of carcinoma - adenoid cystic, adenocarcinoma etc

May become malignant

Usually long standing and recurrent lesions

529
Q

What is a dry socket

A

Alveolar osteitis

Localised inflammatory reaction in bone adjacent to socket

Bone adjacent to socket becomes necrotic and removed by osteoclats

Healing is slow - treatment involves irrigation and antiseptic dressings

Very rarely develops into osteomyelitis

530
Q

Causes of dry socket (5)

A

Excessive rinsing

Fibrinolysis of clot

Poor blood supply due to radiotherapy

Pagets disease

Excessive use of vasoconstrictors

531
Q

What is sclerosing osteitis

A

Focal bone reaction to low grade inflammation

Occur at any age

Commonly affects mandibular molars

Asymptomatic, incidental finding

532
Q

Radiographic features of sclerosing osteitis (2)

A

Uniform opacity at apex of tooth

Often with peripheral lucency

533
Q

Treatment for sclerosing osteitis

A

Address cause of inflammation

534
Q

What is osteomyelitis

A

Inflammation within bone marrow cavities of bone

Occurs following problems with blood supply, host response or other causes including bisphosphonate therapy

535
Q

Aetiology of acute osteomyelitis (3)

A

Most commonly infectious

Extension of periapical abscess

Physical injury/fracture

536
Q

Symptoms in acute osteomyelitis (4)

A

Pain

Pyrexia

Lymphadenopathy

Malaise

537
Q

Histological features of acute osteomyelitis (3)

A

Acute inflammatory infiltrate

Increased bone resorption

Decreased bone formation

538
Q

Aetiology of chronic osteomyelitis (2)

A

Low grade inflammatory reaction

May be progression from acute osteomyelitis

539
Q

Symptoms in chronic osteomyelitis (4)

A

Pain

Swelling

Bone loss

Sequestrae

540
Q

Histological features of chronic osteomyelitis (3)

A

Chronic inflammatory infiltrate

Both osteoclastic and osteoblastic activity

Reversal lines

541
Q

Radiographic features of chronic osteomyelitis (4)

A

Radiolucency with focal opacity

Moth eaten

Indistinct margins

Sequestrae

542
Q

Management of osteomyelitis (3)

A

Resolve source of infection

Remove infected bone

Hyperbaric oxygen

543
Q

Risk factors of osteonecrosis of jaw (5)

A

Diabetes

Smoking

Poor OH

Prolonged drug use

Dental extractions

544
Q

How to manage osteonecrosis of the jaws

A

Prevention - dental assessment, OH, SC, limit alcohol intake

Refer to OS/OMFS

545
Q

Clinical features of benign osteoma (4)

A

Localised bony nodule on maxilla or mandible

Shows continued growth

Distinguish from tori

May be associated with syndromes

546
Q

Histopathological features of benign osteoma

A

Composed of either compact bone and/or cancellous bone

547
Q

Features of osteosarcoma (7)

A

Malignant tumour which produces bone

Rapidly growing swelling

Pain

Nerve involvement

Radiolucency with bone formation

Loss of lamina dura is an important sign

Irregular destruction of bone, permeation of corticaly plate

548
Q

Management of osteosarcoma

A

Wide local excision +/- radiotherapy

549
Q

What is a fibro osseous lesions

A

Lesion where normal bone is replaced by fibrous tissue in which abnormal bone is laid down

550
Q

Radiographic features of a fibrous osseous lesion (2)

A

Radiolucent - bone loss

Mixed lesion with radiopacity - abnormal bone laid down

551
Q

Features of ossifying fibroma (4)

A

Benign neoplasm composed of fibrous tissue which forms spiules, islands or cementicles of bone

May be in craniofacial bones

Premolar/molar region

More in females

552
Q

Histological feature of ossifying fibroma

A

Lesion has a well defined margin and is separated from the cortical bone

553
Q

Patient management of ossifying fibroma (2)

A

Conservative enucleation

Resection

554
Q

Features of fibrous dysplasia (3)

A

Developmental or reactive

Painless smooth enlargement/swelling

Poorly demarcated radiopacity

555
Q

Management of fibrous dysplasia (6)

A

Growth stabilises over time

Debulking and contouring of bone

Recurrence during growth phase

Surgical removal

Orthodontics and orthognathic surgery

Low risk of malignant transformation

556
Q

Features of osseous dysplasia (6)

A

Reactive

Multiple radiopacities in tooth bearing areas of jaw

Composed of irregular trabeculae of woven bone and cementum in fibrous stroma

Focal = single lesions

Periapical = multiple lesions at apex of tooth

Florid = multiple lesions throughout the jaw

557
Q

Features of Pagets disease (5)

A

Bone turnover increased and no longer related to functional demands

Early stages bone becomes vascular - may cause heart failure

Later stages bone becomes sclerotic - shows numerous resting and reversal lines

Clincal - Legs bowed, enlarged skull and jaws (deaf, denture doesnt fit well)

Dental - sclerotic bone = harder extractions, bisphosphonates

558
Q

Key features of fibrous dysplasia (4)

A

Poorly defined lesion

No margin

Males = females

Often maxilla

559
Q

key features ossifying fibroma (4)

A

Well defined lesions

Clear margins

Females > males

Often mandible

560
Q

What are giant cell lesions

A

Characterised by replacement of bone by fibrous tissue containing numerous multinucleated giant cells

561
Q

Features of cherubism (3)

A

Developmental condition

Autosomal dominant trait

Bilateral expansion of posterior mandible

562
Q

Features of central giant cell granuloma (4)

A

Reactive or hyperplastic lesions

Benign but may be locally destructive

Characterised by osteoclasts

Well demarcated radiolucency

563
Q

Management of central giant cell granuloma (3)

A

Blood biochemistry

Curettage

Resection

564
Q

Features of hyperparathyroidism

A

Stones, Bones, Groans, Moans

Radiolucent lesion

Brown tumour - identical to giant cell granuloma

565
Q

Treatment for hyperparathyroidism - browns tumour

A

Treat the hyperparathyroidism - surgery

Oral Disease (1 decks)

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