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BDS5 > Oral Medicine > Flashcards

Oral Medicine Flashcards

1
Q

What is the definition of a: 1) Vesicle? 2) Bulla?

A

1) VESICLE = Small fluid-filled blister (under 5mm) 2) BULLA = Large fluid-filled blister (over 5mm)

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2
Q

What are potential causes of vesiculobullous lesions? (HINT: Pneumonic)

A

ACIDIT(Y)

Auto-immune

  • Pemphigus Vulgaris (intra-epithelial)
  • Dermatitis Herpetiformis (intra-epithelial)
  • Mucous Membrane Pemphigoid (sub-epithelial)
  • Bullous Pemphigoid (sub-epithelial)
  • Linear IgA Disease (sub-epithelial)

Collagen Defect
Epidermolysis Bullosa

Infective

  • HSV1/2
  • VZV
  • Coxsackie A (Hand, Foot & Mouth Disease and Herpangina)

Drugs
PV - ACE Inhibitors & Penicillamine
EM - NSAIDs, Anti-fungals & Barbiturates

Idiopathic

  • ​Erythema Multiforme
  • Angina Bullosa Haemorrhagica

Trauma

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3
Q

What are 7 risks with long-term corticosteroid use?

A
  1. Adrenal insufficiency (ME) - Esp. if abrupt stopping of medication
  2. Hypertension
  3. Skin thinning, bruising & slowed wound healing
  4. Increased susceptibility to infections
  5. Central obesity & peripheral muscle wasting (“orange on a stick”
  6. Cataracts
  7. Diabetes
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4
Q

What is Lichen Planus?

How may it present in different areas of the body?

A

Chronic, Mucocutaneous, PRE-MALIGNANT (0.5-2%) condition - Unknown aetiology (AI?)

ORAL LP (most common, 4-25 years)

  • Symmetrical/Bilateral
  • Asymptomatic or discomfort on spicy/acidic foods
  • Koebner’s Phenomenon (friction/trauma - often post. buccal mucosa, tongue or gingivae)
  • Desquamative Gingivitis (rule out PV/MMP)
  • 6 main types: Papular, Plaque-like, Bullous, Atrophic, Erosive & Reticular

CUTANEOUS LP (transatory, average 18months)

  • Purple Polygonal Pruritic Papules
  • Koebner’s Phenomenon (shins/flexor surfaces)
  • Wickham’s Striae (white striations)

GENITAL LP (20% F & 5% M) - Vulvovaginal- Gingival Syndrome

NAIL (10%) - Dystrophic, Longitudinal grooving, Pitting or Complete loss

SCALP - Scarring alopecia

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5
Q

What is more common Oral or Cutaneous LP?

A

Oral

10-30% OLP have cutaneous lesions

vs.

70-77% Cutaneous LP have OLP

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6
Q

What are the 6 main types of OLP?

A

Purple People Breaking And Entering Raves

  1. Papular (small white papules, may join)
  2. Plaque-like (white patches)
  3. Bullous (blood-filled blister; rare)
  4. Atrophic/Erythematous
  5. Erosive/Ulcerative
  6. Reticular (network of white bands)
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7
Q

What are some differentials for LP?

(Think White patches)

A

Congenital - WSN

Lichenoid Reaction, DLE, Leukoplakia

Infection - Candida (APC or CHC)

Neoplasm - OSCC, Submucous-fibrosis (benign but pre-malignant) or Epithelial Dysplasia

Keratoses - Smokers or Frictional

Other Mucocutaneous conditions: LR, DLE, GvHD

Desquamative Gingivitis: PV or MMP

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8
Q

LP diagnosed through biopsy, what 4 things are seen histologically?

A
  1. Hyperkeratoses
  2. “Saw-like” rete ridges in epidermis
  3. T-Lymphocyte dominant sub-epithelial band
  4. Basal cell liquefaction & degeneration
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9
Q

How is LP managed?

A

No cure & pre-malignant (0.5-2%)

Asymptomatic?

  • Reassure & regular review
  • Warn of malignancy risk: Good OH & Smoking cessation
  • Warn of extra-oral lesions

Symptomatic?

  • Avoid spicy/acidic trigger foods & SLS toothpaste
  • Relieve areas of trauma (cusp tips/ill-fitting denture)
  • Difflam spray (Benzydamine hydrochloride - locally acting NSAID)

MEDS:

1st Line = Topical Corticosteroids (e.g. Hydrocortisone, Betamethasone, Prednisolone)

2nd Line = Topical Immunosuppressants (e.g. Tacrolimus, Ciclosporin)

3rd Line = Systemic Corticosteroids (Prednisolone) or Immunosuppressants (Azathioprine)

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10
Q

How does Lichenoid Reaction present?

In what 5 ways can it be differentiated to LP?

A

Presentation: Similar to OLP

  1. More likely to be erosive (may see ulcerations)
  2. Asymmetrical (if linked to specific materials) but may be bilateral
  3. More likely than OLP to affect palate (also often affects tongue)
  4. Withdrawl of medications/materials show improvement in symptoms
  5. Histologically (similar 4 signs to OLP BUT:
    - Inflammatory infiltrate deeper & less well-defined
    - Large number of plasma cells & eosinophils
    - Pero-vascular infiltrate
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11
Q

What are the 2 main aetiological factors in Lichenoid Reaction?

A
  1. Medication-related
    * ACE Inhibitors, Beta-blockers, Diuretics, NSAIDs, Methyldopa, Hypoglycaemics, Penicillamine, Anti-malarials or Allopurinol (gout tx)*
  2. Material-related
    * Metals (Amalgam/Gold/Nickle) or Resins*
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12
Q

What is the management of Lichenoid Reaction?

A
  • Reassurance - Withdrawl of drug/material if possible & monitor (ensure good history & assertain whether lesion manifestation was linked to changes in medications/restorations)
  • Patch testing locally
  • Manage as LP until lesion resolved
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13
Q

What is Graft vs. Host Disease & how may if present clinically?

What are 2 risk factors?

A

Complication following allogenic bone marrow placement (Immune response)

Acute/chronic forms with oral symptoms often chronic

Clinical Features:

  • White reticular lesions (mimic OLP)
  • Asymptomatic or Burning discomfort
  • Xerostomia (superficial palatal/labial mucoceles)
  • Reduced opening (sclerotic form of GvHD)

2 Risk Factors:
Poorly matched grafts or Older recipients/donors

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14
Q

What is Lupus Erythematous?

What are the 2 main forms?

A

Chronic, Inflammatory Auto-immune disorder

  1. Systemic LE (multisystem, associated with Secondary Sjögrens)
  2. Discoid LE (oral & cutaneous)
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15
Q

What are the oral & cutaneous features of DLE?
How is it managed?

A

Oral:

  • Bilateral distrubution often affecting buccal/labial mucosa, vermillion border or palate
  • Similar to LP but more erythematous.atrophic & reticular (“less well demarcated erythematous areas surrounded by border of white striae”)
  • May ulcerate (active lesion or progression to SLE)

Cutaneous:

  • Scaly red atrophic oval plaques (often on sun-exposed skin) - Well-demarcated with generalised telangiectasia & keratin plugs
  • “Facial butterfly” malar rash
  • Scalp: Scarring alopecia & pigmentation

Management:

ORAL: As with OLP
CUTANEOUS: Suncream (SPF 50), Anti-malarials (Chloroquine) or Steroids

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16
Q

What investigations should be done for SLE/DLE?

What does the histology reveal (6)?

A

Investigations:

  • Biopsy
  • Serology (may see antibodies: Auto-dsDNA & Anti-NA)
  • ‘Lupus Band Test’ (IF staining - often only detects SLE)

Histology:

  • Para or Ortho-keratosis
  • Chronic inflammatory infiltrate in sub-epithelial CT
  • Hyalinisation in sub-epithelial CT
  • Basal layer degeneration/liquefaction
  • Irregular pattern of acanthosis
  • May see: Civatte bodies & Keratotic plugging
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17
Q

What are 8 predisposing factors for Candida infection?

A
  1. Smoking
  2. Poor OHI / Ill-fitting appliance (CEC)
  3. Xerostomia
  4. Long term broad-spec ABx use
  5. Long term Corticosteroid use (esp topical inhalers)
  6. Malnutrition
  7. Uncontrolled DM
  8. Immunosuppression - HIV/Chemotherapy (Cytotoxics) or Age
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18
Q

What are 7 different forms of Candida Infection?

How do they roughly differ?

A
  1. Acute Pseudomembranous (Thrush)
    White/yellow (‘milk curd’) patches - wipe away to leave raw erythematous base
    A**ysymptomatic, often palate or dorsum of tongue
  2. Acute Erythematous
    PAINFUL erythematous lesion on palate/dorsum of tongue (depapillation)
    Often associated with LT Abx use (“ABx sore mouth”) & other general RFs
  3. Chronic Erythematous (Denture Stomatitis)
    Erythematous lesion underlying poorly fitting/unhygienic appliance (often palatal) - Often asymptomatic
    Classified with Newton’s Classification
  4. Chronic Hyperplastic
    White/Erythematous lesion, often affects buccal mucosa (near labial commissures) - DOES NOT RUB OFF
    Homogenous (plaque like) or Non-homogenous (nodular & speckled appearance)
    Must be biopsied as pre-malignant lesion with risk of dysplasia (“Candidal Leukoplakia”)
  5. Chronic Mucocutaneous
    Genetic disorders - AI/Endocrine causing increased susceptibility to candidal infections (widespread white patches which may also affect skin/nails/ other MM)
  6. Angular Cheilitis
    Bilateral red fissuring at labial commissures +/- yellow crusting
    Mixed infection: C. albicans, Staph. aureus & Strep.
    Most common in denture wearers, mask wearers & reduced OVD
  7. Median Rhomboid Glossitis
    Localised erythematous diamond shaped lesion on dorsum of tongue (depapillation) at junction between anterior 2/3rd & posterior 1/3rd tongue
    May have kissing lesion (same on palate) & often asymptomatic - strong association with smokers & LT corticosteroid inhaler use
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19
Q

What are the general special investigations for candida?

(Insert specifics for some types of candida)

A

Special Investigations:

  • Clinical History & See if lesion wipable (APC)
  • FBC & Haematinics
  • HbA1c (ideally <48mmol/mol or <6.5%)
  • Smear/Swab
  • Saliva Culture, Oral Rinse or Imprint Culture (all see fungal load)
  • Biopsy - CHC (pre-malignant, 5-10% Dysplasia)
  • Thyroid function test (may be associated with APS-1 in CMC)
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20
Q

What are the main types of anemia?

How may they present in the mouth?

A

Iron-deficient (often MICRO-cytic)

  • Decreased MCV
  • Glossitis (smooth & de-papillated)
    ROU
    BMS
    Candidal infections
  • Seen in Plummer-Vinson-Kelly Syndrome

Folate or B12-deficient (often MACRO-cyctic)

  • Increased MCV
  • Glossitis (red, raw & beefy)
    ROU
    BMS
    Candidal infections
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21
Q

What is the general management for Candidal infection?

Include specifics for certain types?

A
  • Identify & manage pre-disposing factor
    Smoking cessation?
    Vitamen deficiencies?
    DM management by GMP?
    Corticosteroid inhaler? Advise rinsing after use
  • Ill-fitting denture? (CEC) - Redesign, denture OHI & consider topical miconazole gel under denture or integrated anti-fungal with tissue conditioner
  • Symptomatic? Dietary advice: Avoid spicy/acidic foods & SLS-toothpaste. Eat live active culture yoghurt
  • OHI +/- CHX mouthwash
  • Anti-fungals:
  • Topical = Miconazole (gel) or Nystatin (oral suspension)
    AVOID MICONAZOLE/FLUCONAZOLE in WARFARIN (M/F) & STATINS (M)
  • Systemic = Fluconazole (or Itraconazole etc if resistant)
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22
Q

What might be seen histopathologically in a Candidal infection?

A
  • Epithelial acanthosis & parakeratosis ⇒ Broad, blunt rete ridges
  • Candidal pseudohyphae
  • Chronic inflammatory infiltrate
  • +/- Dysplasia (seen in 5-10% of Chronic Hyperplasic Candidoses - “Candidal Leukoplakia”)
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23
Q

How can Chronic Erythematous Candidosis be classified?

A

Newton’s Classification:

1) Pin-point hyperaemia
2) Diffuse erythema confined to denture fit surface
3) Nodular appearance of palatal mucosa

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24
Q

What are 2 pre-malignant candidal infections?

A
  1. Chronic Hyperplastic Candidosis
  2. Chronic Mucocutaneous Candidosis (associated with OSCC)

(5-10% exhibit epithelial dysplasia & 15% risk of malignant transformation)

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25
Q

What are some differentials for ulcers?

(Pneumonic)

A

So Many Laws And Derivatives

Systemic (BIGS)

  • Blood - Aneamia/Neutropenia/Leukaemia
  • Infection - Bacterial (TB/Syphilis) or Viral (HSV/VZV/HIV)
  • GIT - UC/Crohns/Coeliac
  • Skin - Erosive LP/EM/PV/MMP/Linear IgA/ DH/AB

Malignancy - OSCC, Lymphoma, Kaposi’s Sarcoma

Local - Trauma or Burns

Aphthous/ Aphthous-like - RAS (3) or secondary (e.g. Bechets, Anaemia, Crohns)

Drugs - Nicoranadil (most common, angina), Aspirin or Cytotoxics

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26
Q

What are the 3 main types of RAS?

(How do they differ in terms of ulcer count, size, shape, colour, healing & age onset)

A
  • *1) MINOR** (most common, ~2nd decade)
  • <10mm (1-5 ulcers)
  • oval
  • grey base & erythematous border
  • heal in 1-2wk without scarring
  • non-keratinised (BM)
  • *2) MAJOR** (~1st decade)
  • >10mm (“up to 10 ulcers)
  • irregular/oval
  • grey base +/- induration
  • heal from 2wk-3m WITH scarring
  • keratinised OR non-keratinised (esp. fauces)

3) HERPETIFORM (least common, ~3rd decade)

  • 0.5-3mm (1-20 ulcers)
  • round (may coalesce to become irregular)
  • yellow base with erythematous border
  • heal in 1-2wk WITHOUT scarring
  • non-keratinised (esp. FoM & ventral tongue)
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27
Q

What can generalised recurrent (aphthous-like) ulcers be secondary to?

A
  • Bechets
  • Smoking cessation!
  • Anaemia
  • Immunodefeciency
28
Q

What are the special investigations for ulcers?

A
  1. FBC & Haematinics
  2. Swabs/Cultures
  3. Biopsy (rare, to rule out malignancy)
29
Q

What is the general management for oral ulceration?

A
  • Diagnoses & tx/management of underlying causes
  • Trauma
  • Medications
  • Malnutrition/Vitamin deficiencies
  • Infections
  • Encourage pt to make ulcer diary r/e triggers
  • 1st Line:Pain management - Analgesia (NSAIDs/Paracetamol/Difflam), Diet advice (avoid spicy/acidic food & SLS toothpaste) & Barriers (eg lidocaine)
  • 2nd Line: Topical Steroids
  • 3rd Line: Systemic Steroids
  • 4th Line:
    Colchicine (gout)
    Azathioprine (immunosuppressant)
    Thalidomide (good for HIV/Bechets-related ulcers or LP)
30
Q

What is Beçhets & how may it present?

A

Chronic AI disease affecting small blood vessels

⇒ Triad of aphthous-like recurrent oral ulcers, genical lesions & recurrent eye inflammation

Symptoms:

  • Recurrent oral ulceration (most consistent feature & vital for Beçhets diagnosis)
  • Recurrent genital ulcers
  • Eye lesions (e.g. uveitis or loss of vision)
  • Cutaneous lesions (e.g. erythema nodosum)
  • Joint inflammation
31
Q

How can Beçhet’s Disease be diagnosed?

A

International Clinical Criteria for Bechets Disease Classification:

Must have: Recurrent Apthous Oral Ulceration

And any 2 of the following:

  • Recurrent genital ulceration
  • Eye lesions
  • Skin lesions
  • Positive pathery test (excessive papular reaction observed to needle injury)
32
Q

What are the histological features of Leukoplakia? (6)

Which of these features are shared by Erytheroplakia? (3)

A
  1. Hyper or Para-keratoses
  2. Atrophy (E)
    - Reduced thickness of epithelium
    - Loss of saw-tooth rete ridges
  3. Chronic Inflammatory Infiltrate (e.g. lymphocytes) (E)
  4. Increased thickness of prickle cell layer

May also present with:

  1. Candidal hyphae (~30%)
  2. Features of Dysplasia (E)

(E) = Atrophy, Inflammation & Dysplasia

33
Q

Whats the difference between a pre-malignant lesion & condition?

What are 2 pre-malignant oral lesions & 4 pre-malignant conditions?

A

Premalignant Lesions = Morphologically altered tissue where cancer more likely to occur than in normal counterpart

  1. Leukoplakia (Homogenous/Non-homogenous)
  2. Erythroplakia

Premaligant Oral Conditions = Generalised state associated with increased risk of developing cancer

  1. Oral Lichen Planus (0.5-2%)
  2. Chronic Hyperplastic Candidosis (15%)
  3. Submucous Fibrosis (30%) - may present with trismus
  4. Actinic Keratoses (~6%) - red/white lesion on lowerlip
  5. Patterson-Kelly-Brown Syndrome - Fe deficient anaemia, glossitis, post-cricoid oseophageal web & difficulty swallowing
34
Q

What is Leukoplakia & in what 2 main ways can it present?

How do these presentations differ in terms of risk of malignant change?

A

Leukoplakia = “White patch that cannot be clinically or pathologically characterised as any other disease and is not associated with any causative agents; except smoking tobacco (very common, ~90% cases)” - Diagnoses of exclusion

  1. HOMOGENOUS
    Flat, uniform white patch
    Surface (4) : Smooth, wrinkled pumice-like or corrugated (consistent texture throughout)
    Low malignancy risk (0%)
  2. NON-HOMOGENOUS/ SPECKLED
    White & Red lesion
    Surface (4): Irregular, Nodular, Verrucous (warty) or Exophytic (outwardly growing)
    High malignancy risk (26%)
35
Q

How does erythroplakia present?

How is it managed by the GDP?

What may be seen histologically?

What is the rate of malignant change?

A

Bright red velvety plaques which cannot be characterised as any other definable lesions/diseases.

GDP: Urgent 2 week OMFS referral for biopsy & tx
NICE (2021) H&N Cancers: Recognition & Referral
“Urgent 2week referal for any red/white patch consistent with erythroplakia or erythroleukoplakia”

Histology:

  • Atrophy (loss of rete ridges & thin epidermis)
  • Inflammatory infiltrate
  • Dysplasia! (10)

Rate of malignant change = 80%

36
Q

What are some differentials for red lesions in the mouth?

(using So Many Laws And Derivatives pneumonic)
same as ulcers

A
  • *Systemic:
  • B*leeding disorders ⇒ Bruising, Varices
  • Infection - Candidal AEC/CEC/CMC,MRG or Herpes
  • *G**IT - OFG
  • S**kin - Angina Bullosa Haemorrhagica

Malignancy - Erythroplakia, Kaposi’s Sarcoma, OSCC, & Radiation mucositis

Local - Trauma or Burns

Atrophy - Anaemia, Geographic Tongue, Atrophic OLP or Lupus Erythematosis

Drugs - Anti-retrovitals, Cytotoxic chemotherapeutics, Minocycline,

37
Q

What are 10 histological changes observed in Dysplasia?

Which are most commonly observed in OSCC biopsy?

A
  1. Loss of basal cell polarity
  2. Loss of cell adhesion
  3. Loss of epithelial stratification
  4. Increased nuclear to cytoplasmic ration
  5. Increased abnormal mitoses
  6. Drop-like rete ridges
  7. Pleomorphism
  8. Hyperchromatism (increased DNA content)
  9. Premature keratinisation in prickle cell layer
  10. Mitoses in prickle cell layer

3 down, 2 up - Dipen Patel Has Plentiful Money

38
Q

What are some presentations/clinical features of a potential malignant lesion? (8)

A
  • Persistent, non-healing ulcer (>3wk)
  • Red or Red/White lesions in the mouth
  • Persistent lumps in the oral cavity or lymph nodes
  • Parasthesia
  • Bleeding
  • Mobility of teeth or non-healing socket
  • Changes in voice
  • Difficulty or pain when swallowing

Systemic Features: Unexplained weight loss, malaise or features of distant metastases (main sites = 3 Ls: Lungs, LNs & Liver)

39
Q

What are some of the RED FLAG features of a suspicious oral lesion?

A
  • *SITE:**“Gutter area” - FoM or posterior lateral border of tongue
  • *SIZE:** Larger & rapidly increasing
  • *COLOUR:** Red or Speckled
  • *CONSISTENCY:** Indurated (firm) or Fungation (outgrowths)
  • *SHAPE:**
  • Raised, rolled borders​
  • Nodular
  • Non healing ulcers
  • *SURROUNDINGS:** Destruction or Fixation
  • *SYSTEMIC:**
  • Lymphadenopathy
  • Weight loss
  • Changes in voice or difficulty swallowing
  • Parasethesia, bleeding or mobility
  • Risk Factors: Older, Smoker, Paan, Drinker…
40
Q

What are some special investigations for OSCC?

How can it be graded/staged?

A

Special Investigations:

  • Biopsy - FNA or Incisional (signs of invading dysplasia)
  • Radiographs (assess bony involvement)
  • CT, MRI & PET Scans (assess ST involvement)

TNM Staging:Tumour Nodal metastases Metastases (distant)

  1. ​T(1-4) size & depth of tumour
  2. N(0-3) presence & size of LN containing carcinoma
  3. M(0-1) presence of distant metastases (e.g. lungs)

Based on this allocated Stages 1-4, with reduced prognoses at later stages.

41
Q

What are the treatment options for OSCC? (3)

What might be some long-term complications for the patient?

A

3 Rs of treatment:

  1. Resective & reconstructive surgery
  2. Radio/Chemotherapy
  3. Rehabilitation - Appliances/Speech

Long -term complications:

  • Radiotherapy - Xerostomia (caries/candida), ORN, Osteomyelitis, & Impaired wound healing/Increased bleeding (neutropenia/anaemia/thrombocytopenia)
  • Chemotherapy - MRONJ
  • Difficulties speaking, eating or swallowing
  • Increased risk of pathological fracture (e.g. large mandibular tumour)
42
Q

What are 5 acute oral effects of radiotherapy?

A
  1. Mucositis (should heal 2-3wk post-therapy)
  2. Xerostomia
  3. Changes in taste
  4. Difficulty swallowing
  5. Infection (from state of immunosuppression)
43
Q

What are 6 chronic/long-term oral effects of radiotherapy?

A
  1. Xerostomia
  2. Radiation caries
  3. Difficulty swallowing
  4. Changes in taste
  5. Risk of:
    - ORN (esp. if dosage over 60Gy)
    - Osteomyelitis
    - Pathological fracute
  6. Increased bleeding risk & impaired wound healing (thrombocytopenia/anaemia/neutropenia)
44
Q

What are 5 clinical investigations carried out for suspected PV/MMP?

How can the two be distinguished from these?

A
  1. FBC
  2. Haematinics
  3. HbA1c
  4. Biopsy (Direct IF stain & Histology
  5. Serum (Indirect IF stain)

BIOPSY:
PV ⇒ Positive “Fish net” IF stain
⇒ Intra-epithelial clefting, ancantholysis & ancantholyic “Tzank” cells
MMP ⇒ Characteristic “sub-basilar” split & IgG/C3 deposits at BMZ​

SERUM:
PV ⇒ DSG-1 (& DSG-3) autoantibodies

45
Q

What are 3 differences between PV & MMP?

(Pathogenesis, Clinical features, Histology)

A
  1. PV (INTRA-epithelial) & MMP (sub-epithelial
  2. PV affects oral mucosa or skin
    MMP affects MUCOSA: oral, occular or genital (less often skin)
  3. Biopsy (Direct IF stain & histology)
    PV ⇒ Positive “fish net” IF stain & histological intra-epithelial clefting, acantholysis & acantholytic “Tzank” cells
    MMP ⇒ Characteristic “sub-basilar split” & homogenous linear IgG/C3 deposits at BMZ
46
Q

What is Nikolsky’s Sign? In what conditions may you see it?

A

Fragile lifting of skin epidermis on lateral pressure

Present in: Pemphigus Vulgaris & Mucous Membrane Pemphigoid

47
Q

What is the general management for virus’?

(Include prescription doses as per FGDP 2020 Antimicrobial Prescribing in Dentistry)

A

ARABS MP

Analgesia

Reassurance (often self-limiting)

Anti-virals
TOPICAL: Aciclovir Oral suspension (200mg/5ml) or Cream (5% 5xday)
SYSTEMIC: Aciclovir 200mg 5xD for 5 days)
“Doses change based on clincial presentation & age/immunocompromised status - check BNF”

Bed rest

Soft diet & fluids

Mouthwash (CHX)

Prevention of spread (& NO elective treatment, emergency with reduced aerosols)

48
Q

What is Erythema Multiforme?

What are 4 possible aetiologies?

How does it present orally & cutaneously?

A

Type 3 (hypersensitivity) reaction to:

  1. Infection (70% HSV)
  2. Medications (NSAIDs, Anti-fungals or Barbiturates)
  3. Systemic (e.g. malignancy, SLE or pregnancy)
  4. Idiopathic (50%)

ORAL: Blisters & recurrent ulceration, often affects lips (lip crusting common)
CUTANEOUS: “Target/Iris” lesions, often on extremeties

49
Q

How may Pemphigus Vulgaris present:

  • Orally?
  • Cutaneously?
A

ORAL:

  • Rapidly rupturing blisters & shallow, non healing ulcers
  • Nikolsky’s Sign
  • Desquamative Gingivitis
  • Burning pain/ difficulty swallowing or eating (esp. if oesophagus involvement)

CUTANEOUS:

  • Large, non healing erosions/ulcers (often 3-4m after oral lesions)
50
Q

How may Mucous Membrane Pemphigoid present:

  • Orally?
  • Extra/orally?
A

ORAL:

  • Rapdily rupturing blisters ⇒Painful ulceration (mimics erosive LP)
  • +/- Blood-filled blisters
  • Nikolsky’s Sign
  • Desquamative ginigvitis

EXTRA-ORAL:

  • ​Occular - Chronic Conjunctivitis, Burning, Photophobia, Entopion (eyelid inturning), Trichiasis (eyelash ingrowth) or Blindness
  • Genital - Blisters/ulceration, pain on urination, may scar
51
Q

How may HSV1/2 infection present (2)?

What are 4 trigger factors for its re-activation?

A

Acute/Primary Herpetic Gingivostomatitis

  • More common in children
  • Mucosal vesicles (2-3mm) rupture to painful erosions & heal without scarring (7-10 days)
  • Systemic features: Lymphadenopathy, Pyrexia, Malaise

Herpes Labialis (Cold Sore) - Reactivation

  • Prodromal “tingling” 24hr before lesion
  • Lip vesicle, heals without scarring (~10 days)

Triggers:

  1. Sunlight/UV
  2. Immunosuppression
  3. Infection
  4. Menstruation
52
Q

How may Varicella Zoster Virus present (4)?

A

Chickenpox

  • Itchy maculo-papular rash on skin (back/chest/face) & may be intra-oral (often palate/fauces )
  • Systemic side effects (Lymphadenopathy, Malaise, Pyrexia etc)

Shingles - Reactivation

  • Painful, erythrematous rash (“trunk lesion”) along single dermatome

Post-herpetic (Trigeminal) Neuralgia - CN5 reactivation

  • Burning pain & Allodynia (pain on touch)

Ramsay-Hunt Syndrome - CN7 reactivation

  • LMN facial nerve palsy, vesicular rash (EAM & Palate), Dizziness & loss of taste
53
Q

What are the 3 main types of anaemia?

How may they present? (Oral & Systemic features)

A

1) Iron Deficiency Anaemia ​

  • Smooth & depapillated tongue
  • Brittle & Koilonycia (spoon-shaped) Nails
  • Plummer-Vinson Syndrome
    (Females, Fe-deficient anaemia, Osophogeal post-cricoid web, Difficulty swallowing, Glossitis & Oseophageal cancer risk)

​​2) Pernicious (B12 Deficiency) Anaemia

  • “Hunter’s Glossitis” - Red, beefy, painful depapillaed tongue
  • Peripheral neuropathy

3) Folate Deficiency Anaemia

  • “Hunter’s Glossitis” as above

ALL:

ORAL = Glossitis, RAS, Angular Cheilitis & Burning Mouth

SYSTEMIC = Pallor, Fatigue & Shortness of Breath

54
Q

What are 7 conditions can present with Sialosis (swollen SG)?

A
  1. Sjrogrens Syndrome
  2. Sialolithiasis (SG calculi/stone)
  3. Bacterial Sialadenitis
  4. Viral Sialadentitis (mumps)
  5. Alcoholism
  6. Bulimia
  7. Tumour
55
Q

What are 6 general oral features of malnutrition (vitamin/haematinic deficiencies)?

A
  1. Glossitis
    Fe deficiency = Smooth, depapillated
    B12 & Folate = “Hunter’s Glossitis” (red, raw, beefy, depapillated)
  2. RAS/ROU
  3. Angular Chelitis (+/- other Candidal infections)
  4. Burning Mouth
  5. Delayed wound healing
  6. Increased infection susceptibility

Also: Zinc deficiency (common in elderly) can lead to taste loss/changes

56
Q

What are 8 oral features of Coaeliac Disease?

A
  1. Dental Hypoplasia (96% childhood coaeliacs)
  2. Malnutrition ⇒
    Glossitis
    RAS/ROU
    Angular Chelitis
    Burning Mouth
  3. Exacerbation of Lichen Planus
  4. Other AI diseases (e.g. DM or Sjogren’s Syndrome)
  5. Dermatitis Herpetiformis (oral/cutaneous)
57
Q

What are:

  • 6 specific oral features
  • 6 non-specific oral features

for Crohn’s Disease?

A

SPECIFIC:

  1. Mucosal tag-lesions
  2. Cobble-stone mucosa
  3. Lip swelling
  4. Muco-gingivitis
  5. Deep, linear ulceration
  6. OFG

NON-SPECIFIC:

  1. Glossitis
  2. RAS/ROU
  3. Angular Chelitis
  4. Burning Mouth
  5. Pyostomatitis vegetans (chronic, pustular mucocutaneous disorder, also may be seen in UC)
  6. Persistent submandibular lymphadenopathy
58
Q

What are the 7 main oral features of HIV?

A

How Can We Know Nehete Upset Payne

Hairy Leukoplakia - EBV, white corrigation laterl border of tongue

Candidal infection

Warts - HPV infection (premalignant? HPV16/18 associated with increased OSCC & cervical cancer risk)

Kaposi’s Sarcoma - HHV8 infection, red/purple malignant neoplasm, often on palate, gingivae or skin

Non-Hodgkin’s Lymphoma - WBC malignancy, single, firm painless LN swelling (often on neck)

Ulceration

Periodontitis (ANUG/ANUP) - Bacterial (fusobacterium/spirochete) infection, gingival necrosis/ulceration/punched out lesions/bleeding & halitosis. Systemic features with increased severity.

59
Q

ANUG/ANUP:

  • What is the aetiology?
  • Who is at increased risk? (5)
  • What are the clinial features?
  • How is it treated? (FGDP 2020)
A

Aetiology:
Opportunistic bacterial infection (Fusobacterium & Spirochetes)

Risk Factors:

  • Poor OH
  • Smoker
  • Stress
  • Malnutrition
  • Immunocompromised (e.g. AIDS, Uncontrolled DM or Age extremeties)

Clinical Features:​

  • Gingival ulceration & bleeding (painful)
  • Gingival necrosis - “Punched out” interdental lesions
  • CAL in ANUP
  • Halitosis

Treatment:
- OHI
- Debridement
- CHX m/w
FGDP (2020) Antimicrobial Prescribing in Dentistry
1st Line = Metronidazole (400mg TDS for up to 5 days)
2nd Line = Amoxicillin (500mg TDS for up to 5 days)

60
Q

What is the aetiology & clinical features of Glandular Fever/Infectious Mononucleosis?

How can this diagnosis be confirmed? (3)

A

Aetiology:
EBV Infection

Clinical Features:

  • Faucal oedema & creamy tonsillar exudate - Sore throat
  • Palatal petechiae (30%)
  • Ulceration
  • Systemic: Lymphadenopathy, Malaise, Fever

Diagnosis:

  1. EBV Serology
  2. Monospot Test (+ive)
  3. Paul Bunnell Test (+ive)
61
Q

What is the aetiology of Syphilis? What are some routes of transmission?

What are the 3 main stages & how do they differ in clinical features?

A 
_Aetiology:_ 
Treponema pallidum (bacterial infection)

Routes of Transmission:
Sexual, Sharing of needles or Pre/peri-natal

STAGES:

  1. PRIMARY (21 days after infection)
    Painless “chancre” sores on lips/genitals (heal in 2-6 weeks)
  2. SECONDARY
    Non-specific symptoms: Sore throat, lymphadenopathy, malaise, fever, weightloss & non-itchy rash on skin
  3. TERTIARY
    Oral: Leukoplakia & Palatal “gumma” necrosis
    Life-treatening multi-system invasion
62
Q

What is the “Challacombe Scale” of Oral Dryness?

A

Cumulative score of 1-10 given (increased score = increased severity)

1 pt for each of the following:

  1. Mirror adheres to buccal mucosa
  2. Mirror adheres to tongue
  3. Fissured tongue
  4. Depapillated tongue
  5. Frothy saliva
  6. Lack of salivary pooling
  7. Glassy mucosal appearance
  8. Cervical caries (in 2+ teeth)
  9. Altered gingivae (e.g. smooth)
  10. Debris on teeth or palate

Score of 7-10 = Severe dryness (salivary substitutes & topical fluoride usually needed, further investigation into aetiology & close monitoring warrented)

63
Q

What are 12 possible special investigations for Xerostomia? (&why)

A
  1. Challacombe’s Scale of Oral Dryness
  2. Sialometry - Unstimulated/Stimulated Salivary Flow
    * (<1.5mL in 15 mins = Hyposalivation)*
  3. Schirmer’s Eye Test
    * (<5mm in 5mins = Hypolacrimal flow)*
  4. FBC
  5. Blood Glucose (exclude DM)
  6. Serum
    - ANA, Anti-Ro & Anti-LA (Sjögrens Syndrome)
    - Rheumatoid Factor (Secondary SS)
  7. Sialograph
  8. Ultrasound
  9. MRI
  10. SG Biopsy (minor SG)
  11. Viral/Bacterial Swab or Culture
  12. Chest X-Ray (exclude sarcoidosis)
64
Q

What are potential causes of Xerostomia?

(HINT: Pneumonic)

A

Dehydration & PHARMS

  1. Dehydration - Reduced fluid intake or DM
  2. Psychological - Anxiety
  3. Habits - Mouth breathing)
  4. Age
  5. Radiotherapy
  6. Medication - Anti-convulsants/depressives/hypertensives/histamine Hypnotics, NSAIDs or Cytotoxics
  7. Salivary Gland Disease (DINO)
    Degenerative    (AI - Sjogrens Syndrome)
    Infection (Bacterial/Viral Sialadentitis inc TB)
    Neoplasms (Benign: Pleomorphic Adenoma / Warthin’s Tumour)
    (Malignant: Carcinoma Ex-PA / Mucoepidermoid
    Adenoma / Adenoid Cystic Carci. / Acinic Cell Carci.)
    Obstruction (Sialolithiasis /Mucocele)
65
Q

What are 8 signs & 4 symptoms of Xerostomia?

A

Signs:

  1. Red, atrophic mucosa (“Glassy appearance”)
  2. Mirror adheres to mucosa
  3. Red, depapillaed tongue
  4. Lack of saliva pooling
  5. Frothy saliva
  6. Food debris
  7. Candidal infection
  8. Increased caries (esp. smooth surface)

Symptoms:

  1. Burning/ Soreness
  2. Difficulty: Eating, Swallowing, Speaking or Controlling dentures
  3. Changes in taste
  4. Halitosis
66
Q

What are 5 Qs you would want to ask a pt in relation to their Xerostomia?

A
  1. How long have you had daily sensation of dry mouth?
  2. How many L/glasses of fluids do you drink a day?
  3. Do you wake up in the night to drink fluids?
  4. Have you had recurrent/persistent SG swelling?
  5. What medications do you take - Any similar onset of symptoms?
  6. Have you had any other areas of mucosal dryness (E.g. eyes/ genitals - SS)
67
Q

What are 2 benign & 4 malignant Salivary Gland neoplasms?

A

Benign:

  1. Pleomorphic Adenoma
    Most common, often in Parotid or Minor SG
    High recurrence rate (incomplete capsule structure)
    ~6% malignant transformation
  2. Warthin’s Tumour
    Almost exclusive to Parotid gland
    Low recurrence rate

Malignant:

  1. Carcinoma Ex-Pleomorphic Adenoma
  2. Mucoepidermoid Carcinoma
  3. Adenoid Cystic Carcinoma
  4. Acinic Cell Carcinoma

BDS5 (5 decks)

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