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Oral Diseases > Theme 6 - oral ulceration and mucocutaneous lesions > Flashcards

Theme 6 - oral ulceration and mucocutaneous lesions Flashcards

1
Q

What is oral lichen planus?

A

Common chronic inflammatory disorder affecting stratified squamous epithelia. Typically are small white papules that often coalesce and form lines (Whickham’s striae). Typically bilateral, F>M, 50-60years old.

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2
Q

What are the clinical features of oral lichen planus?

A
  • Bilateral but not always symmetrical
  • Spontaneous exacerbations and improvements
  • Striations and erythematous change
  • Posterior buccal mucosa most frequent site followed by tongue, gingiva, labial mucosa and lower lip
  • Palate, FoM and upper lip uncommon
  • Lesions migrant and can spread
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3
Q

In white OLP, describe the following types and their differential diagnosis:
a) Papular oral lichen planus
b) Reticular oral lichen planus
c) Plaque like oral lichen planus

A

a) Small white patches on buccal mucosa. DD = fordyce granules (these are more yellow)
b) Most common appearance, white striations, pt unaware of presence. DD = oral lichenoid lesions, geographic stomatitis
c) Long lasting striations that have coalesced to form patches. DD = leukoplakia, proliferative verrucous leukoplakia (PVL)

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4
Q

What are 5 things that would suggest it is oral lichen planus?

A

1) Multifocal lesions
2) Papules and/or striae can be seen
3) Lesions involve dorsum of tongue
4) Typical cyclical course
5) Histology suggestive

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5
Q

In Red OLP, describe the following:
a) Atrophic (erythematous) OLP
b) Erosive and bullous OLP

A

a) Erythematous lesions that affect the gingiva cause dequamative gingivitis. Frequently involve dorsum of tongue. Discomfort.

b)Erosions and straitions, unusual to see blistering. Intense pain and burning. Hardly remit spontaneously and may lead to confusion wuth other autoimmune mucosal blistering diseases e.g. PV

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6
Q

What are the extra-oral manifestations of OLP?

A

Cutaneous lesions:
-can develop within several months after appearance of oral lesions
- Usually erythematous to violaceous papules that are flat-topped
- Most commonly volar wrists and forearms
- Self-limiting and cause itching

Genital LP:
- Genital mucosa affected in women with OLP = vulvovaginal-gingival syndrome
- Burning, pain, vaginal discharge, dyspareunia
- Penogingival syndrome less common, malignant change has been reported

Scalp:
- Planopilaris - causes scarring and alopecia

Nails:
- Nail plate damage, onycholysis, longitudinal striation

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7
Q

What is the histopathology of OLP?

A
  • Hyperkeratosis
  • Basal cell liquification with apoptotic cells
  • Band like inflammatory infiltrate (T-lymphocytes)
  • Absence of epithelial dysplasia
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8
Q

What is the pathogenesis of OLP?

A

T cell mediated autoimmune disease which CD8 and T cells trigger apoptosis of oral epithelial cells

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9
Q

What is the classification of lichen planus and lichenoid lesions?

A

Oral lichen planus
Oral lichenoid lesions:
- Oral lichenoid contact lesion (OLCL)
- Oral lichenoid drug reaction (OLDR)
- Graft vs host disease - oral lichenoid lesion (GVHD-OLL)

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10
Q

Why is biopsy and histological diagnosis of OLP/OLL recommended? What cannot be reliably distinguished?

A

To exclude dysplasia or maligancy
Histopathology cannot reliably distinguish between OLP and OLL

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11
Q

What is the etiology of OLP/OLL?

A
  • Genetic predisposition (cytokine polymorphisms)
  • Dental materials (amalgam)
  • Viruses (mainly HCV - liver disease associated with LP)
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12
Q

How can you distinguish oral lichenoid contact lesion and oral lichen planus?

A

OLCL has close contact relationship with fillings.
Is not bilateral/symmetrical

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13
Q

What is the evidence for dental materials causing OLCL?

A

Amalgam components, friction and plaque should be considered.
Replacement of amalgams can result in improvement but not all

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14
Q

What is lichenoid dysplasia? What is its aetiology>

A

Oral lichen planus could be a premalignant condition - dysplasia with lichenoid features. OLP pts have increased risk of developing oral cancer so must be followed up.
Aetiology:
- Erosive variety
- Smoking, alcohol
- Viruses (HPV, HCV)
- OLP therapy
- Candida
- Diet

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15
Q

In the oral mucosa, what is the
a) mucosa
b) submucosa
made up of?

A

a) Lining, epithelium, lamina propria (layer of connective tissue)
b) Fibrous and adipose tissue, minor salivary glands, neurovascular bundles

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16
Q

What is the difference between
a) Masticatory mucosa
b) Lining mucosa
c) Specialised mucosa
and where are they each found?

A

a) Keratinised epithelium: Keratin layer, granular cell layer (loss of organelles), prickle cell layer (desmosomes anchor cells together), basal cell layer. Found gingivae and hard palate
b) Non keratinised epithelium. Found labial and buccal mucosa, ventrum of tongue, FOM, soft palate
c) Keratinised epithelium. Found dorsum of tongue, filiform, fungiform and circumvallate papillae

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17
Q

Both clinically look like white patches, but what is the histology of
a) Hyperkeratosis
b) Hyperorthokeratosis

A

a) Retained nucleus in keratinised layer
b) No nuclei, excessive thickness

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18
Q

What are the 3 white lesions due to ketatosis of the oral cavity that are hereditary?

A

1) White sponge naevus:
- Bilateral and symmetrical usually on BM
- Raised shaggy white plaque
- Autosomal dominant - mutation to keratin 4 and 13

2) Genodermatoses ie inherited skin conditions
- Dyskeratosis congenita (increased risk of SCC, seen in young when LP unusual! Skin hyperpigmentation, anaemia, thrombocytopenia etc)
- Tylosis (increased oesophageal cancer risk, hyperkeratosis palms and soles)
- Follicular keratosis (Darier’s disease)

3) Pachyonychia congenita
- Palmar plantar keratosis
- Gross thickening of nails
- Keratosis of oral cavity
- Similar to white sponge naevus but skin lesions
- Autosomal dominant

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19
Q

What are the 3 white lesions due to keratosis that occur from trauma?

A

1) Frictional keratosis
- Cheek/lip chewing chronic e.g. linear alba

2) Chemical trauma
- Aspirin burn
- Oil of cloves
- Denture cleanser

3) Smokers keratosis
- chemical and thermal
- White plaques and melanosis (brown pigmentation)
- Inflamed salivary glands

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20
Q

What are the 4 white lesions due to keratosis that occur from infections?

A

1) Syphilis (Treponema palidium)
- Sites: dorsum of tongue, syphilitic glossitis, syphilis leukoplakia
- Snail tracks and mucous patches = secondary, atrophic glossitis = tertiary
- Hutchinson incisor and mulberry molars
- Risk of malignant change

2) Chronic hyperplastic candidiasis
- White patches not rubbed off
- Sites: commissures, BM, lips tongue palate
- Antifungals don’t work
- Risk of malignant change (cellular atypia)
- Remember pseudomembranous candida are the white patches that wipe off

3) Hairy leukoplakia
- HIV patients/immunosuppression
- Site: lateral border of tongue
- Vertical white folds - corrugated
- Associated with EBV and candida
- No evidence of maliganant change

4) Squamous cell papilloma
- Lip, junction of hard/soft palate
- Common
- HPV
- Soft, painless lesion with fingerlike surface projections, pedunculated and asophytic (grow outwards)

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21
Q

What are the 2 white lesions due to keratosis that occur from dermatological causes?

A

1) Lichen planus
- Type IV hypersensitivity - T cell triggered
- Reticular, plaque like or papular
- Erosive, atrophic, desquamative gingivitis
- Can have skin and genital lesions

2) Lupus erythematosus
- Discoid or systemic
- F>M
- Auto-immune disease type III hypersensitivity
- Multisystem: skin, joints, kidney, cardiac, pulmonary, neuro
- Butterfly rash

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22
Q

What is a white lesion due to keratosis that occurs idiopathically?

A

Leukoplakia

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23
Q

What is oral epithelial dysplasia?

A

Used to describe histological changes that suggest increased risk of malignant transformation in oral potentially malignant disorders. Recognises features of cytological and architectural atypia

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24
Q

What is a) Homogenous leukoplakia and b) Non-homogenous leukoplakia

A

a) Asymptomatic uniform smooth surface, sharp demarcated, shallow fissures
b) Diverse appearance, speckled red/white, nodular, verrucous. Carries a higher risk of malignant transformation

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25
Q

If a patient presents with leukoplakia what is important to find out from their social history and why? What other features are important when predicting risk of malignant progression?

A

If ever smoked. If a non-smoker may have more aggressive course
Size, red specked, buccal mucosa tongue and FOM high risk sites

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26
Q

What is erythroplakia?

A

Fiery red patch, sharply demarcated, flat or depressed. Erythematous mucosa with matt appearance. Unilateral isolated high suspicion of dysplasia

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27
Q

What is the differential diagnoses for a red patch in the mouth?

A
  • Erythroplakia
  • Denture induced stomatitis
  • Erosive LP
  • Pemphigus vulgaris
  • Erythema migrans/geographic tongue
  • Erythematous candida
  • Discoid lupus
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28
Q

What is proliferative verrucous leukoplakia?

A

Multifocal oral leukoplakia with progressive course, starting as one patch then confluence. Frequently gingivae, alveolar process and palate. No erythema or ulceration. Histologically: verrucous, hyperkeratotic, lichenoid, dysplasia
Has the highest risk of malignant change

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29
Q

What is oral submucous fibrosis?

A

Blanching of mucosa, loss of tongue papillae, fibrous bands, tongue rigidity, shrunken uvula, trismus. Associated with betel nut chewing. Fibrosis of the lamina propria.

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30
Q

Does OLP and lichenoid lesions have malignant potential?

A

Yes - if biopsy shows dysplasia then it should be called OLP with dysplasia

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31
Q

What is oral lupus erythematous?

A

Chronic autoimmune disease: systemic, drug induced or discoid.
Similar to OLP but may present with central erythema with surrounding straie whereas OLP more disorganised
Malignant potential - carcinomas rare and most often on lips

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32
Q

What is oral graft vs host disease (GvHD)?

A

Chronic form more likely to cause oral lesions. Result of allogenic haematopoetitic cell transplantation for malignant and non malignant conditions. Can manifest as scleroderma like changes, mucoceles, ulceration, OLP looking.
Can progress to oral cancer

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33
Q

What is reverse smoking and what lesions does it cause?

A

Palatal lesions as a result of holding the burning end of a cigarette in the mouth - malignancy on hard palate. thickened white plaque or erythroleukoplakia, erythema of salivary gland orifices

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34
Q

What is dyskeratosis congenita?

A

Rare hereditary condition. Triad of oral leukoplakia, hyperpigmentation of skin, nail dystrophy. Prognosis poor: malignant change in oral lesions or bone marrow failure

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35
Q

What is the pathway for mild epithelial dysplasia?

A

Routine monitoring for 5 years or if risk factors then oral epithelial dysplasia clinic for close monitoring, re biopsy or resection

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36
Q

What is the treatment for oral graft vs host disease?

A

Like OLP - topical steroid and topical calcineurin inhibitors e.g. tacrolides. On top of immunosuppression

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37
Q

What is the clinical presentation of recurrent aphthous stomatitis?

A
  • Superficial oral mucosal ulceration
  • Recurrent
  • No obvious local cause
  • Self-limited
  • Otherwise healthy individual
  • Usually on non-keratinising oral epithelum
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38
Q

What is the diagnostic criteria for minor RAS?

A
  • Round or oval shaped
  • 2-10mm in diameter
  • Usually 1-5 per crop
  • Predominantly on non-keratinised mucosa
  • Heal without scarring
  • Last 7-14 days
  • Have peri-ulcer erythema in early stages
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39
Q

What is the diagnostic criteria for major RAS?

A
  • Round or oval shaped
  • 10+mm in diameter
  • Usually 1-2 per crop
  • Predominantly on non-keratinised mucosa
  • Heal with scarring
  • Last 14+ days
  • Variable peri-ulcer erythema
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40
Q

What is the diagnostic criteria for herpetiform RAS?

A
  • Round or oval shaped merging to form irreglar shapes
  • Initially less than 2mm in diameter
  • Usually 10+ per crop
  • Occurs on both keratinised and non-keratinised mucosa
  • Heal with or without scarring
  • Last 7-21 days
  • Have peri-ulcer erythema
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41
Q

What is complex aphthosis?

A

Presence of almost constant multiple oral or oral and genital aphthae in the absence fo systemic manifestations

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42
Q

What is the aetiology of RAS?

A
  • Genetics (family history)
  • Haematinic deficiency e.g. iron, folic acid, vit B1, B2, B6 and B12 def
  • Gluten sensitive enteropathy
  • Food allergy e.g. chocolate, coffee, peanuts
  • Sex hormones e.g. occasional improvement with pregnancy
  • Drugs e.g. NSAIDs and B Blockers, nicorandil may cause major aphthae
  • Psychiatric illness
  • Immunodeficiency (humoral and cellular)
  • Infections e.g. bacteria, viruses
  • Local trauma (white halo)
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43
Q

How is RAS diagnosed?

A

Exclusion of other causes
FBC, ferritin, vit B12, red cell folate

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44
Q

What are apthous-like ulcerations (ALU)?

A

Oral ulcerations that run a more complex clinical course requiring more extensive medical screening and management than RAS

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45
Q

What diseases are apthous-like ulcerations (ALU) related to?

A
  • Becets disease
  • MAGIC syndrome
  • Reiters syndrome
  • Cyclic neutropenia
  • PDAPA syndrome
  • Inflammatory bowel diseases
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46
Q

What is cyclic neutropenia?
What is its presentation?

A

Periodic decrease in the circulating neutrophil numbers from normal to very low. Autosomal dominant inherited. Usually recurs every 21 days and lasts 3-5 days

Presentation
- Recurrent infection of the sinuses, respiratory tract and skin
- Inflammation of the throat and gums
- Apthous like ulcers in mouth and colon
- Recurrent fever
- Abdominal pain

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47
Q

What is periodic fever adenitis pharyngitis apthous ulcer syndrome (PFAPA)?
What is its presentation?

A

Recurrent fever occuring every 3-6 weeks, lasting 3-5 days. Pharyngitis. Cervical adenitis. Aphthous stomatitis.

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48
Q

How is PFAPA diagnosed?

A

1) Regularly recurring fevers with early age of onset
2) Aphthous stomatitis, cervical lymphadenitis, pharyngitis
3) Completely asymptomatic between episodes
4) Normal growth and development
5) Exclusion of cyclic neutropenia with blood test

49
Q

What is mouth and genital ulcers with inflamed cartilage (MAGIC syndrome)?
How is it diagnosed?

A

An overlap of Becets disease and relapsing polychondritis

Diagnosis at least 3 criteria:
- Bilateral auricular chondritis
- Serum negative non-erosive inflammatory polyarthritis
- Nasal chondritis
- Ocular inflammation
- Respiratory tract chondritis
- Audiovestibular lesion

50
Q

What is Behcets disease?

A

Multisystem inflammatory disorder characterised by recurrent apthous ulcers, occluar inflammation and involves joints, skin, CNS and GIT. Chronic condition and goes through phases

51
Q

What is the diagnostic criteria for Becets disease?

A

1) Recurrent oral ulceration (at least 3x year) plus one of the following:
2) Recurrent genital ulceration
3) Eye lesions
4) Skin lesions
5) Positive pathergy test

Or point system, oral genital and ocular score 2, skin neuro and vascular score 1. 4+ = becets

52
Q

What is the epidemiology for Becets disease?

A

Common in Turkey and Middle East
Onset 30-40 years
Slightly higher M>F

53
Q

What is the difference between Becets disease and RAS?

A

In becets
- More agressive ulcers
- Major apthous like ulcers more common
- Involvement of multiple sites more common
- Involvement of soft palate and oropharynx more common

54
Q

How is Becets disease diagnosed?

A

Presence of aphthae
FBC
Erytrocyte sedimentation rate (ESR)
C-reactive protein (CRP)
Referral to dermatology, opthalmology, gastroenterology, neurology and reumathology when appropriate

55
Q

What is the management of Becets disease?

A

Topical corticosteroids for oral and genital ulcers. Colchicine orally for skin lesions

56
Q

What is the difference between pemphigus and pemphigoid?

A

Pemphigus = intra epithelial blister - altered adhesion between keratinocytes (acantholysis). Intercellular depositis of IgG and C3 in immunofluorescence.
Pemphigoid = subepithelial blister - altered adhesion at BMZ

57
Q

What are the target antigens of
a) Pemphigus vulgaris
b) Pemphigus foliaceus
c) Paraneoplastic pemphigus
d) IgA Pemphigus?

A

a) DSG3 (desmoglein)
b) DSG1
c) DSG 3
d) DSC1 (desmocollin)

58
Q

What is the epidemiology of pemphigus vulgaris?

A
  • M=F
  • More common 30-60years
  • Meditarranean/Jewish ancestry (HLA-DR4 = ashkenazi Jews)
  • Potentially lethal - but prognosis involving oral cavity significantly better than that of mucotaneous PV
59
Q

What is the aetology of pemphigus vulgaris?

A
  • Drugs containing sulfhydryl radical (thiol drugs) e.g. penicillamine and captopril
  • Non-thiol drugs e.g. rifampicin, NSAIDs, ACE-inhibitora, interferons
  • Physical agents e.g. heat, ionising rays
  • Viruses (herpesviridae)
  • Pesticides
  • Diet (garlic)
  • Stress
60
Q

What are the clinical features of pemhigus vulgaris?

A
  • Onset usually involved oral cavity, lesions run chronic course.
    -Exclusive gingival lesions may appear at onset as isolated blisters and/or erosions of free gingivae
    -Red erosions/ulcerations mainly BM, palate and lips.
    -Minor insult to any uninvolved oral tissue may cause blister (Nikolsky’s sign)
    -Lesions heal without scarring
  • Advanced = severe desquamative gingivitis
  • Ulcerations may affect other mucous membranes e.g. conjunctiva, nasal mucosa, pharynx, larync, skin, genitalia
  • Cutaneous lesions commonly affect skin of head and neck first, bleed easily and crust
61
Q

What is paraneoplastic pemphigus? What is it associated with?

A

Associated with neolplasia mainly B-cell lymohoproliferative disorders:
- Non Hodgkin lymphoma
- Chronic lymphocytic leukaemia
- Castlemans disease
- Thyoma
- Sarcomas
- Waldenstrom macroglobulinemia

62
Q

What are the clinical features of paraneoplastic pemphigus?

A
  • Erosions of oral cavity more severe than in PV
  • Skin lesions - blistering and erosive, can have lichenoid features, can be targetoid, polymorphic, histology may show acantholosis
  • Involvement of bronchopulmonary tree
  • Final diagnosis based on circulating autoantibodies
63
Q

Which types of pemphigus have predominant skin involvement and predominant oral involvement?

A

Skin:
- Pemphigus foliaceus
Oral:
- Pemphigus vulgaris
- Paraneoplastic pemphigus

64
Q

What types of pemphigoid have predominant skin involvement and predominant oral involvement?

A

Skin:
- Bullous pemphigoid
- Herpes gestationis
Oral:
- Mucous membrane pemphigoid

65
Q

What is mucous membrane pemphigoid?

A

A group of autoimmune crhonic inflammatory sub-epithelial blistering diseases affecting mucous membranes characterised by linear depositon of IgG, IgA or C3 along epithelial BMZ

66
Q

What is the epidemiology of mucous membrane pemphigoid?

A

Av age 52-61years
F>M
Very rare in childhood

67
Q

What is the clinical hallmark of mucous membrane pemphigoid?
What places have the highest frequency of involvement?

A

Scarring
Oral - ocular - nasal - anogenital - skin - laryngeal - esophageal

68
Q

What are the clinical features of mucous membrane pemphigoid?

A
  • Most pt have oral lesions, chronic course, gingiva, BM, palate, alveolar ridge, tongue as erythematous patches, blisters erosions
  • Nikolskys sign may be positive
  • Ocular involvement, sight theratening, begins as non-specific conjunctivitis, shortening of fornices then symblepharon (adhesion of eyelid to eyeball), entropion (inversion of eyelid), ankyloblepharon (fusion of eyelid), blindness
  • Skin can be eczematous like or recurrent blisters
69
Q

What are the differential diagnoses for bullous diseases?

A

Erythema multiforme
Ulcerative lichen planus
RAS
Lupus erythematosus
Theraml/chemical burns
I/O herpes simplex
Orofactial granulomatosis
SCC
Plasmacell stomatitis

70
Q

What is erythema multiforme?

A

Uncommon acute usually self-limiting inflammatory disorder affecting skin and mucous membranes

71
Q

What is the classification of erythema multiforme?
a) Oral EM
b) EM minor
c) EM makor/steven johnson syndrome
d) Toxic epidermal necrolysis

A

a) 1-3 weeks, oral erosions/ulcers, no skin, usually lip with crust
b) 1-4 weeks, typical target lesions, at one site usually mouth, mild-sever erythema erosions and ulcers. >10% body SA
c) 1-6 weeks. At least 2 mucosal sites. >30% body involved, target lesions, oral lesions widespread and severe
d) 1-3 weeks - poorly defined erythematous macules and flat targets. Severe mucosal lesions, >30% body SA involved, systemic symptoms poor prognosis

72
Q

What is the epidemiology of erythema multiforme?

A

Adolescent or young males mainly affected. Must have HLA gene testing before giving drugs

73
Q

What are the clinical features of erythema multiforme?

A
  • Oral involvement - early = erythematous spots which progress to blisters that break and for ulcers/erosions
  • Swollen cracked lips with erisons
  • Classic target lesion on skin, extremities usuall involved with symmetric distribution, unusual on face neck and trunk
  • In TEN skin lesions have irregular edges and lack oedematous ring
74
Q

How is erythema multiforme diagnosed?

A
  • Detailed MH ( role of drugs, herpes)
  • Biopsy and DIF and IIF helpful to exclude other diseases.
  • Serology
  • HLA testing
  • Histologically can mimic pemphigoid/pemphigus
75
Q

What is the treatment for erythema multiforme?

A

-Withdraw cause
-Oral EM = topical corticosteroids
- Short course coricosteroids e.g. 50mg prednisolone x3 days then 25 mg next 3 days
- If HSV associated the 6 moth trial antiviral therapy with acyclovir
- If resistant to prednisolone reconsider diagnosis or add azathioprine, mycophenolate mofetil or dapsone

76
Q

What is Nikolsky’s sign in bullous disease?

A

Blow air and detachment of gingivae

77
Q

What tissue test should be done with a patient that has suspected bullous disease? What should then be carried out on these?

A

Biopsy, DIF (differentiates PV from MMP
Serum test, IIF - diagnoses PV standard, split skin to diagnose MMP
ELISA
Immunoprecipitation

78
Q

What is orofacial granulomatosis?

A

Chronic granulomatous inflammation predominant cell type is activated macrophage in oral and maxillofacial region

79
Q

What are the non-infectious types of orofacial granulomatosis?

A

Idiopathic OFG
Crohns disease
Melkerson-Rosenthal syndrome
Cheilitis granulomatosa
Sarcoidosis
Wegeners granulomatosis
Foreign body reaction

80
Q

What are the infectious types of orofacial granulomatosis?

A

Tuberculosis
Tertiary syphilis
Mycotic granulomatous infection
Parasites

81
Q

What is crohns disease? What is its epidemiology?

A

Bowel inflammatory condition primarily affecting distal portion of small bowel and proximal colon. F>M, 20-40 years, 60-80 years

82
Q

What is the aetiology of crohns disease?

A

Genetic susceptibility
Environmental/microbial factors e.g. smoking, diat, mycobacterium avium paratuberculosis, drugs e.g. oral contraceptive, NSAIDs
Immune response - CD4 TH1 reaction induced

83
Q

What are the clinical features of Crohns disease?

A

GI signs - cramping diarrhoea pain fever weight loss anaemia
Oral lesions - non specific = angular cheilitis, apthous like oral ulcers, chronic stomatitis. Specific = diffuse or nodular swelling, cobblestone mucosa, linear ulcers, mucosal tags, erythema/swelling on gingivae
Peripheral atheritis
Skin - erythema nodosum, pyoderma gangrenosum
Eyes - conjunctivitis

84
Q

How is crohns disease diagnosed?

A

1) History
2) Physical exam
3) Elevated EST and C reactive protein
4) Radiographic MRI and endoscopic findings
5) Antibodies anti-saccharomyces cerevisiae serological markers
6) Biopsy

85
Q

What is Melkersson-Rosenthal Syndrome?

A

Clinical traid of lesions:
1) Persistent swelling of oro-facial tissues
2) Fissured tongue
3) Facial paralysis
2/3 signs accepted for Dx

86
Q

What is cheilitis granulomatosa?

A

Limited form of MR more common than complete triad.
Generally painless enlargement of one or both lips, mainly young adults
DD angioedema

87
Q

What is idiopathic orofacial granulomatous?

A

Cases that are restricted to oral cavity without any identifiable know granulomatous disease, usully involving lips. May progress to Crohns disease

88
Q

What is the aetiology of Melkersson-rosenthal and idiopathic OFG?

A

Most cases idiopathic
Hypersensitivity to food substances
Hypersensitivity to dental materios
Infectious ages: mycobacteria, spirochetes, borrelia burgdorferi

89
Q

How is the diagnosis of Melkersson-rosenthal and idiopathic OFG made?

A

Biopsy - in early stages only oedema, indistinguishable from sarcoidosis or crohns. Stains for mycobacteria and fungal organisms recommended

90
Q

What is the management of Melkersson-rosenthal and idiopathic OFG?

A

Elimination diet
Topical corticosteroid (little effect)
Cheiloplastly (recurrence)

91
Q

What is Wegener’s Granulomatosis?

A

Uncommon multi-system disorder, pathological triad:
1) Necrotising granulomatous lesions in upper or lower respiratory tract
2) Systemic vasculitis involving small arteries and vein
3) necrotising glomerulonephritis
If untreated it is fatal

92
Q

What are the signs and symptoms of Wegener’s Granulomatosis?

A

Pulmonary symptoms e.g. cough
Hearing loss
Renal involvement
Oral lesions but rarely presenting feature - hyperplastic granular gingivitis (strawberry gingivitis)
Tooth mobility, poor healing after extraction, cranial nerve palsy, parotid swelling

93
Q

How is Wegener’s granulomatosis diagnosed?

A

2 of the following:
1) Oral ulcers or nasal discharge
2) Presence of nodules or cavities on a chest xray
3) Nephritic urinary sediment
4) Granulomatous inflammation on biopsy
Serological markers and biopsy

94
Q

What is sarcoidosis?

A

Multisystem disorder, young and middle aged adults, more likely women

95
Q

What is the aetiology of sarcoidosis?

A

-Infectious agents: mycobacterium tuberculosis main culprit. Fungal and viral agents
-Organic particles: wood burning particles
-Inorganic agents: insecticides
- Immune response

96
Q

What are the clinical features of sarcoidosis?

A

Acute forms:
- Lofgrens syndrome = fever, erythema nodosim, arthralgia
- Heerfordt-Waldenstrom syndrome =fever, parotid gland enlargement, anterior uveitis, facial nerve palsy
Asymptomatic forms:
- Lung invovement
Eyes - acute uveitis, keratoconjuctivitis, sicca, retinal vascultitis
Skin - erythema nodosum, lupus pernio, maculopapular eruption, subcutaneous nodules
Oro-facial very rare - ST swelling, major salivary gland enlargement
Hypercalcaemia
Liver
Neurosarcoidosis

97
Q

How is sarcoidosis diagnosed?

A

Diagnosis without biopsy with Lofgrens Syndrome
Biopsy from involved organ e.g. skin, LN, SG, oral mucosa

98
Q

What can a foreign body reaction be caused by and what can they cause to the body?

A

Food particles of plant origin
Dental materials - abrasives, polishing and dental restorative material
Silicone mainly in liquid form

Painful and erythematous lesions of gingiva and orofacial swelling. Evidence of granulomatous inflammation and presence of floreing materials

99
Q

If a biopsy is taken and there is a granulomatous reaction with ziehl-neelson negative, what would the follwoing suggest?
a) Gastro-intestinal involvement
b) history of foreign material
c) No systemic symptoms or facial palsy
d) granuloma and respiratory symptoms
e) necrosis and vasculitis, respiratory symptoms and hearing loss

A

a) Crohns
b) Foreign body granuloma
c) Cheilitis granulomatosa/MRS/isiopathic OFG
d) Sarcoidosis
e) Wegener

100
Q

What could be the causes of localised pigmentation of the oral mucous membrane?

A
  • Amalgam tattoo
  • Graphite tattoo
  • Freckles/ephelides
  • Melanotic macules
  • Naevi
  • Melanoma
101
Q

What could be the causes of diffuse pigmentation of the oral mucous membrane?

A
  • Racial pigmentation
  • Somkers melanosis
  • Drug induced pigmentation
  • Peutz-Jeghers Syndrome
  • Laugier-Hunziker syndrome
  • Addison disease
102
Q

What is an amalgam tattoo? How do they occur and what are the clinical features?

A

Introduced during condensation of amalgam fillings, fragments fall away during tooth XTN and fall into open extraction sockets, leaching of retrofilled endo tooth
Pigment greyish/blue, located on gingivae, alveolar mucosa and buccal mucosa

103
Q

What is a graphite tattoo?

A

Black or grey, usually on hard palate from pencil lead.

104
Q

What are melanotic macules?

A

Focal macular pigmentations on the vermillion border of lips, palate, gingivae and buccal mucosa, dont darken after sun exposure, usually brown, F>M. Commonly solitary lesion, no malignant potential. Histologically shows increased melanin pigmentation in basal cell layer.

105
Q

What are naevi? Explain their development

A

Proliferation of melanocytes
a) Junctional naevi - originate as basal layer melanocytes that proliferate in lower strata of epithelium along the junction with connective tissue
b) Compound naevi - later the melanocytes drop off into the connective tissue to form islands
c) Intradermal or intramucosal naevi - eventual fate is to leave the surface epithelium entirely so all the clusters of naevus cells reside in the dermis or submucosa

106
Q

What are the clinical features of naevi?

A
  • Primarily on hard palate, BM and vermillion border
  • Varying size and shades (can be blue)
  • Around 2/3 are raised
  • Malignant potential not determined, excision advised
107
Q

What is a melanoma? What is its epidemiology?

A

Agressive malignant tumour of melanocytes
Rare, 1% of all melanomas arise in oral mucosa. 20-80 years M>F Prognosis poor

108
Q

What are the clinical features of a melanoma?

A
  • 75% cases on hard palate or maxillary gingivae
  • Asymptomatic pigmented patches or plaques with assymmetrical irreguar borders
  • Superficial melanoma = aradial growth phase
  • Invasive melanoma = vertical growth phase
  • May represent metastatic rather than primary lesions
  • Can be rapidly enlarging nodules resulting in ulceration, bleeding, pain and loosening of teeth
109
Q

What are the clinical features of racial pigmentation?

A

Pigmented macules of various configurations , usually diffuse and bilaterally located
Light to dark brown
Gingivae most common then BM, lips, palate, fungiform papillae

110
Q

What is smokers melanosis?

A

Patchy brown macular pigmentation present BM in heavy smokers
Macules 0.5-1cm, multiple and bilateral
Basilar melanosis without melanocyte proliferation

111
Q

What is peutz-jeghers syndrome? Why is it important to diagnose?

A

Mucotaneous hyperpigmentation (pigmented macules, confluent, varying size and shades of brown, lips and BM) and GI hamartomatous polyposisis - inherited autosomal dominant

Any adult pts with longstanding pigmented oral macules require gastroenterology investigation to look for polyps - these can undergo malignant transformation and metastasise to breast testicles and ovaries

112
Q

What is laugier-hunziker syndrome?

A
113
Q

What is Addisons disease?

A

Primary adrenocortical insufficiency resulting from deficit of cortisol and aldsterone production by the adrenal glands.

114
Q

What are the clinical manifestations of addisons disease?

A
  • Malaise
  • Postural hypertension
  • Nausea
  • Anorexia
  • Pigmentation - darkening of skin and mucous membranes due to increased circulating adrenocorticotrophic hormone (ACTH)
115
Q

What are the likely drugs that cause drug induced pigmentation if the colour is
a) Greyish-blue
b) Brown
or if the patient has c) HIV

A

a) Antimalarials, amiodarone, clofazimine
b) ACTH, chemotherapeutic agents, oral contraceptives, phenothiazine
c) Azidothymide and ketoconazole

116
Q

What does the drug imatinib mesylate that is used in the management of onco-haematological conditions such as myeloid leukaemia do to the oral cavity?

A

Pigmentation (usually blue)

116
Q

What does the drug imatinib mesylate that is used in the management of onco-haematological conditions such as myeloid leukaemia do to the oral cavity?

A

Pigmentation (usually blue)

117
Q

What is the differential diagnosis for pemphigus vulgaris oral lesions/ what else do they look like?

A

MMP
Erythema multiforme
Erosive LP
Herpetic stomatitis
Self injury/thermal burn

Oral Diseases (12 decks)

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