Oral Medicine Flashcards
Name the 4 categories of medcinies used in Oral Medicine (OM)?
Anti-microbial - virals, fungals and biotics
Topical Steroids - inhaled and mouthwash
Dry mouth medication - benzdamine wash
Others - carbamazepine
Name the 5 classification of medicines?
General Sales
Pharmacy Medicines
Prescription only Medicines
Controlled Drugs
Medical Devices
What is the definition of a licensed medication?
A medicine that has been proven in evidence to the MHRA to have efficacy and
safety at defined doses in a child and/or adult population when treating specified
medical conditions
Clinical trial data provided
Post licence surveilence via MHRA
What is the defintiion of an unlicensed medication?
Medicines that have not had evidence of efficacy submitted for the condition under
treatment
Will be ‘licenced medicines’ – but for another condition
Use is at the discretion of the treating physician
Patient must be informed that medicine is being used ‘off-licence’
Patient must be given PIL specific to the condition under treatment
Name antimicrobials used for OM? and what they treat?
virals - primary herpetic gingivostomatosis, recurrent herpetic lesions and shingles
- aciclovir
fungals - Acute pseudomembranous candidiasis and acute erythematous candidiasis
- miconazle
- fluconazole
- nystain
Name topical steroids used for OM? and what they treat?
Betamethasone mouthwash
Beclomethasone Metered Dose Inhaler
Both used for
- Treating aphthous ulcers
- Treating Lichen planus
What is the definition of a medical devices?
‘Medical device’ means any instrument, apparatus, implement, machine, appliance, implant, reagent for in vitro use,
software, material or other similar or related article, intended by the manufacturer to be used, alone or in combination, for
human beings, for one or more of the specific medical purpose
- diagnosis, prevention, monitoring, treatment or alleviation of disease,
• diagnosis, monitoring, treatment, alleviation of or compensation for an injury,
• investigation, replacement, modification, or support of the anatomy or of a physiological process,
• supporting or sustaining life,
• control of conception,
• disinfection of medical devices
• providing information by means of in vitro examination of specimens derived from the human body
Medical devices include dry mouth treatments - name 5 types of treatments?
Salivix pastilles
Saliva orthana
Biotene Oral Balance
Artificial Saliva DPF
Glandosane
Name 6 other medicines used in OM?
Tricyclic Antidepressants
Gabapentin/Pregabalin
Azathioprine
Mycophenolate
Hydroxycholoroquine
Colchicine
What needs to be considered before any drug is prescribed or drug is reccomended?
Clinical indication
Licenced or unlicensed for this use
Dose and route of administration
Important warnings for the patient
Drug interactions and cautions
Treatment duration and monitoring
What to include on a presciption?
Patient’s name, Address, Age (under 18)
Patient identifier – DoB, CHI Number
Number of Days treatment
Drug to be prescribed
Drug formulation and Dosage
Instructions on quantity to be dispensed
Instructions to be given to the patient
Signed – identifier of Prescriber
What are the rules and regulation on prescrption validity?
Six months from date issued
More than one item on a script
More than one repeated dispensing occasion
Tips for writing a prescription?
Key Patient information MUST be legible
AVOID abbreviations – write full instructions in INK
Only legal requirement is for dentist to SIGN prescription – this confirms all the
other information is correct and has been checked.
Essentially the SAME information for Private
– GDC number usually added
What are the advantages of written instruction for the patient?
Stressed patient may not remember instructions
Language issues may prevent proper understanding
Multilingual options, large print options
Contact number for Patient Issues with the medicine
Legal protection if post-treatment course questioned
What advice should you give to your patient after prescribing the drug?
Take drugs at correct time and finish the course
Unexpected reactions: STOP! and contact prescriber
Known side-effects should be discussed e.g. Metronidazole and alcohol
Keep medicines safe: especially from children
Types of drugs for mucosal disease?
Non-steroid topical therapy
- inconvientient lesions with discomfort
Steroid topical therapy
- disabling immunologically driven lesions
Non-steroid topical therapy for mucosal diease? - Name 4?
Chlorhexidene mouthwash
- dilute 50% with water if needed
Benzdamine mouthwash or spray
- green things help! Useful topical anaesthetic/pain relief
OTC remedies such as Igloo, Listerine, Bonjela
Anything else the patient finds helpful!
- check that it is not harmful though – bleach, aspirin!
Steroid topical therapy for mucosal diease? - Name 3?
Hydrocortisone mucoadhesive pellet
Betamethasone mouthwash
Beclomethasone Metered Dose Inhaler (MDI/Puffer) -
- CFC-free preparations, e.g. ‘Clenil Modulite’
How does it work - hydrocortisone mucoadhesive tablet?
allow tablet to dissolve over the ulcer
How to use betamethasone mouthwash?
Unlicenced product
• Supply patient with a tailored information leaflet
Use Betnesol tabs 0.5mg
- 1mg 2 tablets
- 10mls water 2 teaspoons water
- 2 mins rinsing
- Twice daily
Refrain from eating/drinking for 30 min after use
DO NOT SWALLOW
Do not rinse after use
What must be included on betamethasone mouthwash PIL?
Licenced for other medical conditions
Explain dose range and frequency of use
Explain hazards of exceeding the standard dose
Add any known side effects – small oral candida risk
Add special instructions
How to use beclomethasone medical device?
Unlicenced product
- Supply patient with a tailored information leaflet
Dental Prescribing 50mcg/puff device
- Position device correctly – exit vent directly over ulcer area
- 2 puffs
- 2-4 times daily
- Don’t rinse after use
Must be a pressurised device
What must be included on beclomethasone medical device PIL?
This is an accepted and proven effective treatment for the oral condition
Licensed for other medical conditions – asthma and COPD
Instruct to discard the manufacturer’s PiL
Explain dose range and frequency of use
Explain technique used for oral lesions – different from use for lung conditions
Add any known side effects – small oral candida risk
Add special instructions
Systemic drugs used in OM, only for specialists?
Disease modulator
- colchine
Steroid
- prednisilone (ulcers) 30mg for 5 days
Immune suppressants:
- hydroxychloroquine - lichen planus
- azathioprine
- mycophenolate
Immunotherapy:
- adalimumab
- enterecept
Systemic use of steroid risk - side effects?
If prolonged course – or repeated short courses over many months
• 3 months continuous
• Gaps of 2 weeks or less between ‘pulses’ of prednisolone.
Adrenal suppression – steroid dependency – don’t stop suddenly – taper dose
Cushingoid features
Osteoporosis risk – bone prophylaxis – Calcium supps and bisphosphonates
- DEXA bone density scan may be needed from time to time
Peptic ulcer risk – Proton Pump Inhibitor prophylaxis
Mood/Sleep alteration and mania/depression risk – can be very quick onset
What preparation do patients need for systemic immunomodulatory treatmets?
Must ensure that immunosuppression will not harm the patient
Pre-existing medical condition not yet detected
Screening for:
Blood borne virus screen
- Hep B, Hep C, HIV
• FBC
• Electrolytes
• Liver Function tests
• Thiopurine Methyltransferase (TPMT)
- Only for Azathioprine use
• Zoster antibody screen
• EBV
• Chest X-Ray
- Evidence of previous/active TB
• Cervical Smear up to date
• Pregnancy test
What must be included when planning immunomodulatory treatment?
Needs full consent from patient
- Alternative treatments tried or discussed
Patient information given and patient reviewed to discuss this
- Short term risk – acute drug reaction
- Long term risk – cancer risk increased – Azathioprine and skin cancer especially
- Effective Contraception to be used and any pregnancy planned with clinical care team
Treatment outcome understood by patient and clinician
- Complete remission, acceptable level of symptoms
- Trial treatment – perhaps 6 months then reassess benefit/need for treatment
What are the differential diagnoses of oral white lesions? 5 examples?
Hereditary
Smoking/frictional
Lichen planus
- lupus erythematosus
- gvhd
Candidal leukoplakia
Carcinoma
What does a typical white spot lesion look like?
Thickening of the mucosa or keratin
- Less visibility of blood
Less blood in the tissues
- vasoconstrictor
What is the definition of Leukoplakia?
A white patch which cannot be scraped off or attributed to any other cause
No histopathological connotation
- it is a clinical description
Diagnosis of exclusion
1 - 5% become malignant
Name 4 types of leukoplakia?
Fordyce’s spots
Smoker’s Keratosis
Frictional Keratosis
Hereditary Keratosis
What is the link between smoking and leukoplakia?
Smokers are six times more likely to have “leukoplakia”
Low malignant potential of the lesion
- But higher oral cancer risk overall!
Name 3 types of infective leukoplakia?
Candidosis
- pseudomembranous acute (thrush)
- denture associated (chronic)
Herpes Simplex
When should you refer a white spot lesion?
Most are benign
If RED and WHITE concentrate on the RED part
If the lesion is becoming more raised and thickened
If the lesion is ‘without cause’
- lateral tongue
- anterior floor of mouth
- soft palate area
Why are red spot lesions red?
Blood flow increases
- inflammation
- dysplasia
Reduced thickness of the epithelium
What is the definition of Erythroplakia?
Atrophic or non-keratotic end of the spectrum
A red patch which cannot be attributed to any other cause
More of a concern for malignancy than leukoplakia
Why does a red/blue lesion look like it does? explain why?
Fluid in the connective tissue
- Dark – slow moving blood – varicosities
- veins or cavernous haemangioma
Light Blue – clear fluid
- saliva (mucocele), Lymph (Lymphangioma)
Name 2 types of vascular hamartomas?
Haemangioma
- capillary
- cavernous
What is thw defintion of a lymphangioma?
Lymphangioma
- most are cavernous
Tongue
- cystic hygroma
Name 3 types of connective tissue diseases?
Large vessel Disease
- giant cell (temporal) arteritis
Medium Vessel Disease
- polyarteritis nodosa
- kawasaki disease
Small vessel Disease
- granulomatosis with Polyangiitis
What are the 3 types of mucosal pigmentations?
Exogenous stain
Intrinsic Pigmentation
Intrinsic foreign body
Name the 4 examples of exogenous stains for mucosal pigmentation?
Tea
coffee
chlorhexidine
Bacterial overgrowth
Name the 4 examples of intrinsic pigmentation for mucosal pigmentation?
Reactive Melanosis/melanotic macule
Melanocytic naevus
Melanoma
Effect of systemic disease - paraneoplastic phenomenon
Name the 1 examples of intrinsic foriegn body for mucosal pigmentation?
Metals
Name the differential diagnoses for brown/black lesions - localised and generalsied?
Localised:
- Amalgam
- Melanotic Macule
- Melanotic naevus
-Malignant Melanoma
- Peutz-Jehger’s syndrome
- Pigmentary incontinence
- Kaposi’s sarcoma
Generalised:
- Racial/familial
- Smoking
- Drugs
- Addison’s disease (Raised ACTH conditions)
Name 2 types of melanin pigmentation?
Racial pigmentation
Melanotic macule
What questions to think about when deciding whether to refer for mucosal pigmentations?
Is it easily explained?
- Racial
- Smoking
- Medicines
Is it increasing in size, colour or quantity?
Any NEW systemic problem?
Do I have an EXISTING radiograph showing it to be amalgam?
What is the ateiolog of mucosal inflammation?
trauma - physical or chemical
infection - viral, bacterial or fungal
immunological
can be remalignant or melignant
How to decide whether something is a melanoma? questions?
Variable pigmentation
Irregular outline
Raised surface
Symptomatic
- Itch
- bleed
What is the purpose of a biopsy?
identifies or excludes malignancy
identifies dysplasia
identifies other disease, e.g. lichen planus
When must you biopsy?
if unexplained
When should a patient be referred to oral medicine?
Patients with abnormal and/or unexplained changes to the oral mucosa
- Practitioner threshold will vary with experience
If there is concern about dysplasia risk
- Appearance of lesion
- Risk site
- Risk behavior
- Family history
When should you NOT refer a patient to Oral Medicine?
Asymptomatic VARIATIONS of NORMAL mucosa
Benign conditions the practitioner has diagnosed that:
- Are asymptomatic
- Do not have potentially malignant risk
- For which there is no treatment
If unsure – consider clinical photography to
- Monitor area until next check up
- Send to specialist for an opinion
When should a mucsoal lesion be refered to oral medicine for an opinion?
ANYTHING the dentist thinks is might be cancer or dysplasia
- 2 week Cancer referral pathway for actual malignancies
- NICE and SIGN Head & Neck cancers guidelines
Any SYMPTOMATIC lesion that hasnot responded to standard treatment
- Hospital referral criteria
- SDCEP guidance
Any BENIGN lesion that the patient can’t be persuaded is not cancer…..
What is the oral mucosa made up of?
stratified squamous epithelium
lamina propria
gross types
- lining, masticatory, gustatory
microscopic
- non-keratinised
- keratinised
- orthokeratosis or parakeratosis
Different parts of the mouth which are keratinised and non-keratinised?
Keratinised - palate
Non-keratinised - cheek
What are the compartments of the oral mucosa?
STratum
Corneum
Granulosum
Spinosum
Basal
Lamina Properia
Cornified, Maturation, Progenitor
Name the 3 reactive chnages of the oral epithelium?
Keratosis
- nonkeratinised site
(parakeratosis)
Acanthosis
- hyperplasia of
stratum spinosum
Elongated rete ridges
- hyperplasia of basal cells
Name the 5 mucosal reactions of the oral mucosa?
Atrophy - reduction in viable layers
Erosion - partial thickness loss
Ulceration - fibrin on surface
Oedema - intracellular
- intercellular (spongiosis)
Blister - vesicle or bulla
How do age and nutritiona ffect the oral mucosa?
Age - progressive mucosal atrophy
Nutritional deficiency
- iron or B group vitamins
- atrophy
- predisposes to infection
Name 3 types of benign tongue conditions? Dorsal surface
Geographic tongue
- 1-2% of population - less in children
- desquamation - varied pattern and timing
Black hairy tongue
- hyperplasia of papillae
- bacterial pigment
Fissured tongue (scrotal tongue)
What are the symptoms of geographic tongue?
Sensitive with acidic/spicy foods
Intermittent
Much worse in young children
What is the aetiology of geographic tongue?
None!
Something else is causing the trouble
- Haematinic deficiency (B12, Folate, Ferritin)
- Parafunctional trauma
- Dysaesthesia
How to manage a black hairy tongue?
Sucking on a peach stone
What is the definition of a fissued tongue?
Fissured tongue is a benign condition characterized by deep grooves (fissures) in the dorsum of the tongue.
Although these grooves may look unsettling, the condition is usually painless.
Some individuals may complain of an associated burning sensation
The cause is unknown, but it may be partly a genetic trait. Aging and environmental factors may also contribute to the appearance
Is there another disease process there?
- Candida
- Lichen planus
What is the defintion of glossitis? And possible investigations?
What is Glossitis?
- Glossitis can mean soreness of the tongue, or more usually inflammation with depapillation of the dorsal surface of the tongue (loss of the lingual papillae), leaving a smooth and erythematous (reddened) surface
What investigations are needed?
- Haematinics
- Fungal cultures
What is the definition of black hairy tongue?
is a condition of the tongue in which the small bumps on the tongue elongate with black or brown discoloration, giving a black and hairy appearance.
What is the aetiology of black hairy tongue?
smoking,
xerostomia (dry mouth),
soft diet,
poor oral hygiene
certain medications
What is the aetiology of glossitis?
Often caused by nutritional deficiencies
- Fe
- B
- Infection
- others
When should you refer a swelling to Oral Medicine?
Symptomatic (pain is a feature of salivary gland malignancy!)
Abnormal overlying and surrounding mucosa
Increasing in size
‘rubbery’ consistency
Trauma from teeth
Unsightly
What is the definition of a pyogenic granuloma?
granulation tissue – mixed inflammatory infiltrate on fibro-vascular background
any mucosal site response to trauma
Not a granuloma, not pyogenic
other names
- gingiva – aka vascular epulis
most frequent site
- gingiva, during pregnancy
pregnancy epulis
Name the 5 causes of mucosal ulcerative reactions?
Trauma
Immunological
Infections
GI
Carcinoma
Name the differential diagnoses for immunological and GI mucosal ulcerative reactions?
Immunological:
- aphthous ulcers
- lichen planus
- Lupus
- vesiculo-bullous
- Erythema multiforme
GI:
- Crohn’s
- UC
What are the differential diagnoses for single episode oral ulceration?
Trauma
1st episode of Recurrent Oral Ulceration
Primary Viral infections
Oral Squamous Cell Carcinoma
What are the differential diagnoses for Recurrent Oral Ulceration?
Aphthous ulceration
- minor, major, herpetiform
Lichen Planus
Vesiculobullous lesions
- pemphigoid, pemphigus
- angina bullosa haemorrhagica
- erythema multiforme
Recurrent viral lesion – HSV, VZV
Trauma
Systemic disease – Crohn’s Disease ulceration
Describe the difference between Crohn’s ulcers and aphthous ulcers?
Aphthous-type ulcers:
- haematinic deficiency associated
- behave like aphthous ulcers
Crohn’s specific ulcers:
- linear at the depth of the sulcus
- full of Crohn’s associated granulomas
- persist for months – intralesional steroids help
Explain what to include for an Oral Ulceration History?
Where?
Size & Shape?
Blister or ulcer?
How long for?
- more than 2 weeks?
Recurrent?
- same site? different Sites?
Painful?
Explain how to describe/examine an ulcer?
Margins?
- flat? raised? rolled?
Base?
- soft? firm? hard?
Surrounding tissue
- inflamed? normal?
Systemic Illness?
What is the definition of traumatic ulceration?
Common
Usually single episode
- can be recurrent if cause not removed
Normal or abnormal epithelium
Healing
- remove cause
- heal in about 2 weeks
Describe a recurrent herpetic lesion? - location and treatment
Ulceration limited to one nerve group/branch
Often Hard palate
- lesion recurs in the same place
- patient often aware of prodrome and vesiculation which bursts
- PAIN suggests Herpes ZOSTER rather than
simplex
Treat with systemic ACICLOVIR
- prophylactic if a severe problem
Describe recurrent aphthous stomatitis (RAS)? severity? diagnosis?
Severity:
- minor
- major
- herpetiform
- Behçet’s syndrome
Diagnosis by :
- history
- examination
What is the general rule for recurrent self-healing ulcers?
Those affecting exclusively the non-keratinized mucosa are inevitably aphthae.
The overall summary of Oral Ulceration?
Not all ulcers are aphthous!
Is the lesion on keratinized or non-keratinized mucosa
Are there systemic symptoms?
- consider infection – herpes group, coxsackie group
Always look for a traumatic cause
- primary – sharp edge on a tooth/appliance
- secondary – parafunction rubbing mucosa against the teeth
What is the definition of an Aphthous Ulcer?
- Immunologically generated RECURRING oral ulcers
- Follow a set pattern depending upon the ulcer type
- Genetically driven with environmental modification
- Multifactorial environmental triggers and variable expression
- Ulcer experience may change as ‘risk factors’ change over life
Describe the characteristics of a minor aphthous ulcers?
- Less than 10mm diameter
- Last up to 2 weeks
- ONLY affect NON-Keratinised mucosa
- Heal without scarring
- Usually a good response to topical steroids
This is the commonest type of recurrent oral ulceration
- One is a nuisance, many more at once can be disabling
The ULCER FREE PERIOD is a good guide to morbitity
– longer ulcer free + less morbidity
Describe the characteristics of a major aphthous ulcers?
- Can last for months
- Can affect ANY part of the oral mucosa
- keratinised OR non keratinised or both - MAY scar when healing
- Poorly responsive to topical steroids
- intralesional steroids often more useful
Usually LARGER than 10mm
- may get smaller ulcers too – diagnose from the worst ulcer
Describe the characteristics of a herpetiform aphthae ulcer?
- Rarest form of Aphthous ulcers
- Multiple small ulcers on non-keratinized mucosa
- Heal within 2 weeks
Can coalesce into larger areas of ulceration
NOTHING to do with herpes viruses
- in the early stages looks like primary herpetic gingivostomatitis
- in HSV get KERATINISED epithelium involved – not in herpetiform aphthae
What cause Oral and Genital Ulceration?
Behçet’s Disease (mainly)
Vesiculobullous diseases
Lichen Planus
How to diagnose Behcet’s disease?
Many who don’t meet the criteria
Diagnosis
- three episodes of mouth ulcers in a year
- at least two of the following: genital sores, eye inflammation, skin ulcers, pathergy
What is the definition of Behcet’s Disease? and where can it effect?
PRIMARILY a Vasculitis – inflammation of blood vessels
- Oral & genital ulceration
- Eye disease
- snterior or posterior uveitis – can lead to loss of vision in 20% - Bowel ulceration – iliocaecal area – pain and cramping
- Heart and lungs
- Brain
- Joints
How to manage a patient with Behcet’s Disease?
Treat local oral disease or RAS
Systemic immunomodulation where multisystem involvement:
- Colchicine used ‘off label’ often a first treatment
- Azathioprine/Mycophenolate
- Biologics – infliximab and others
Managed with help of Rheumatology
- also National specialist treatment centres
Name the 7 predisposing factors for Recurrent Aphthous Stomatitis (RAS)?
Viral and bacterial infections
Genetic predisposition
Systemic diseases
Stress
Mechanical injuries
Hormonal level fluctuations
Microelement deficiences
What to remember for Aphthous ulcers?
Damage happen before the ulcer appears
- treatment is most effective in ulcer rpodrome period
What tests to carry out when investigating aphthous ulcers?
Blood test:
- haematinic deficiencies Iron B12 or folic acid
- coeliac disease
- TTG (tissue transgutaminase)
- if TTg +ve anti-glidain and anti-endomysial abs
Allergy tests - contact or immediate hypersensitivty
- food additives E210-E219
- benzoate
- sorbate
- cinnamon
- chocolate
Explain the treatment of a recurrent Aphthae?
Management:
Correct blood deficiencies
- ferritin (iron), folic Acid, vit B12
Refer for investigation if Coeliac positive
- endoscopy and jejunal biopsy
Avoid dietary triggers
- SLS containing toothpaste – (Sensodyne Pronamel and Kingfisher are SLS free)
Dietary triggers
- identified from testing
- empirical dietary avoidance – use FOOD MAESTRO app to help with identifying foods
Explain the treatment of a recurrent Aphthae?
Management:
Correct blood deficiencies
- ferritin (iron), folic Acid, vit B12
Refer for investigation if Coeliac positive
- endoscopy and jejunal biopsy
Avoid dietary triggers
- SLS containing toothpaste – (Sensodyne Pronamel and Kingfisher are SLS free)
Dietary triggers
- identified from testing
- empirical dietary avoidance – use FOOD MAESTRO app to help with identifying foods
What drugs can be prescribed for aphthous ulcers?
In dental practice follow SDCEP ’Drugs in Dentistry’ Guidance
Non-Steroid Topical Therapy
- for inconvenient lesions
Steroid Topical Therapy
- for disabling lesions
Why do chuildren get aphthous ulcers?
Periods of rapid growth – very few before this
- 8-11 years and 13-16 years
- feet usually grow first so look for ‘new shoe sign’
Treatment
- usually respond to 3/12 iron supplements – always check the diet for peculiarities
NOT related to growth (present since birth) then largely a genetic component:
- consider allergy testing as well as bloods
Treatment:
- issues with Betnesol under age 12 - licence
- issues with Betnesol if child unable to spit mouthrinse out reliably
When should you refer an Aphthous ulcer case?
After simple investigations
After topical trreatment
If no good result has been achieved
If patient under 12 YO
What is the defintion of oral thrush?
Caused by candida
Can be associated with dentures causing denture stomatitis
What species of candida causes oral thrush?
Candida albicans
Name the 10 host factors that predispose you to developing oral thrush?
Immunosuppression
Endocrine disorders
Nutritional deficiency
Antibiotics
Steroids
Female
Extremes of age
Hospitalisation
Smoking
High carb diet
Name the 5 intraoral factors that predispose you to oral thrush?
Poor oral hygiene
Salivary gland dysfunction
Oral mucosal damage
Dental prosthesis
Changes to commensal flora
Name the topical and systemic treatment of oral thrush?
Topical:
- nystatin
- miconazole
Systemic:
- fluconazole
- targeted therapy
Explain how to use nystatin suspension?
1ml QDS
Keep in mouth for as long as possible
Continue for 48 hours after resolved
Low risk for inters
Explain how tonuse miconazole oral gel?
2.5 ml QDS - gold in mouth after food
Continue for 7 days after resolved
Use gel to brush dentures
What treatment is advised for angular cheilitis?
Miconazole
- antifungal
- bacteriostatic vs gram positive
- topical
- with mild steroid
Name the drug interactions of Miconazole?
Inhjbits the metabolism of drugs metabolised by the CYP3A4 and CYP 2C9 enzyme systems
CYP3A4:
- statins
- Ca ch blocker
- tacrolimus
- carbamazepine
- midazolam
CYP2C9
- warfarin
- sulphonylureas
- phenytoin
Name the contraindications of miconazole?
Liver dysfunction
Coadministration with drugs that are metabolised by CYP3A4
Substrates known to prolong QT interval - astemizole, cisapride, dofetilide, mizolastine, pimozide, quinidine, sertindole and terfenadine
Ergot alkaloids
HMG-CoA reductase inhibitors - simvastatin
Triazolam and oral midazolam
Explain how to take fluconazole?
50-200mg capsules
50-5ml oral suspension
IV avaliable
50mg once a day for 7-14 days
100mg if immunocompromised
Name the 6 contraindications of fluconazole?
Mod inhib of P3A4 and 2C9
Strong inhib of 2C19
Alfentanil
Amitriptyline
Benzodiazepines
Citalopram
Clopidogrel
Warfarin
How importance is drug resistance to antifungal?
A growing problems
Most common in azoles
Explain a dentists role in antimicrobial stewardship?
Don’t start antibiotics without bacterial infection
Use local guidelines
Document everything such as indication, duration, dose and route
Review clinical diagnosis and the need for the pt to continue the dose 48 hours after symptoms go
Name 7 types of oral symptoms?
Dry mouth
Oral discomfort
Taste disturbance
Difficulty chewing
Difficulty swallowing
Difficuly speaking
Halitosis
Advice for toothbrushing?
At least twice a day
Small headed brush
Medium texture filament
Soft brush if very sore
Toothpaste between 1350-1550 ppm Fl
Water if toothpaste is unworkable
How can a nurse care for a patients teeth if they can’t?
Twice daily brushing
Gloves with toothpaste
Small circular motions
Start on outer surfaces then move to inner surfaces
Spit out toothpaste after brushing
Avoid rinsing
How can a nurse care for a patients denture?
Cleanse denture after meals
Cleaned and removed overnight
Ensure denture fits well
Adhesive if necessary
How can a nurse care for a patients soft tissue?
Glove and run finger over tissues
Renew gause on cleansing
Can use cleaning stock if gause not good
Record mouth condition
How can a nurse care for a patients lips?
Moisten with water
Apply saliva replacement
Or apply aqueous cream BP
What to implement for a dry or coated mouth patient?
At least 4 x a day
Review medicines
Gently remove coating, debris and plaque
Maintain hydration
Stimulate saliva
Which 5drug types cause dry mouth?
Opoids
Anticholinergics
Antidepressants
Diuretics
Oxygen
Explain how to manage dry mouth?
Treat underlying cause
Review medication
Good oral hygiene
Dietary advice
Regular dental checks
Regular sips of water
Lubricate cracked lips
Saliva substitutes
Saliva stimulants
What does saliva consist of?
6.8-7.4 pH
Water
Mucin-principal active component
Electrolytes
Enzymes
Proteins
Name saliva stimulants?
Sugar free chewing gum or sweets
Frozen fruit juices or lollies
Organic acids such as salivix pastilles
Describe artifical saliva?
Mucon or carboxymethylcellulose based
Short duration of action
Avoid acidic products - glandosane
Neutral pH
- AS saliva Orthana
- Biothene Oralbalance gel
- BioXtra gel
- Saliveze
Which saliva replacements can a dentist prescribed on the NHS?
Glandosane
Saliveze
Salivix pastilles
Salivox Plus pastilles
At what age does lichen planus usually affect?
30-50 years old
What percentage of skin and oral cases are there.
50% oral lesions
10-30% skin lesions
Name the main types of Lichen Planus and their
Cutaneous - skin
Reticular - commonest
Erosive - premalignant
Desqamative attached gingivae
Descriptors - Atrophic/Ulcerated/ Plaque
What is the histopathological findings of lichenoid reaction?
Chronic inflammatory cell infiltrate
Saw tooth rete ridges
Badal cell damage
Patchy acanthosis
Parakeratosis
What is the histopathological findings of licehn planus?
Orthokerstosis
Wedge shaped hypergrabulosis
Dermal epidermal Junction obscured lymphocytes
Vacuoles at basal later
Luck band of lymphocytes under epidermis
Civatte bodies - dead keratinocytes
What does the histopathological findings tell us?
Lymphocyte activation
Overreaction to normal trigger
Virus umplicated in immune upregulation but NOT as a cause of LP - hep C or herpes
Sometimes has external triggers - medicines or amalgam
What are the 8 aetiologices of lichen planus
Autoimmune
Viral
Genetic predisposition
Physical and emotional stress
Trauma - scraped or after surgery an isomorphic response (koebnerisation)
Localised skin disease - herpes zoster - isotopic response
Contact allergy - amalgam
Drugs - gold, quinine, beta blockers and ACE inhibitors
What are the symptoms of lichen planus?
Often none
May relate to thinning of epithelium
- sensitive to hot and spicy food
- burning sensation in the mucosa
What other body parts can LP affect?
Skin
Scalp
Genitals
Hair
Nails
What are the 5 main sites for oral LP?
Biccal mucosa
Gingiva - desquamative gingivitis
Tongue- lateral or dorsum
Lips
Palate
Describe buccal lichen planus?
Commonest
Can be found anywhere
- ant at commisure
- mid
- post around 3rd molar
Mainly an incidental finding
Easy to biopsy
Describe gingival lichen planus?
Found in isolation
Termed desquamative gingivitis
- similar to gingival pemphigoid and to plasma cell gingivitis - clear histological
Very erythematous appearance to the gingiva
Patchy
Reticular pattern more common
Oral hygiene is essential to settle the lesion - plaque driven
- especially interdentally
Biopsy can be difficult
- risk of damage to attachment area
- adherent attached mucosa damaged lifting from bone
Describe tongue lichen planus?
Dorsum usually idiopathic
- loss of papillary becoming smooth
Lateral may be drug/amalgam trigger
- amalgam most likely in isolated lesion
- look at tongue rest position - contact amalgam?
Easy biopsy but painful
Describe lip lichen planus?
On the lip
Biopsy hard?
Looks sore
Erythema
What is it called if the cause is known for oral lesion?
Lichenoid reaction to…
Medications which can cause LP?
ACE inhib
Beta blockers
Diuretics - bendroflu and frusemide
NSAIDs
DMARDs
Rare - phenothiazines
Name 3 types of DMARDs?
Penicillamine
Gold
Sulphasalazine
What are the discriminative characteristics of a lichenoid drug reaction?
Widespread lesion
Bilateral and mirrors
Poorly response to standard steroid treatment
How to manage lichenoid drug reactions?
Benefit of the drug vs the risk of stopping the drug
How bad is the discomfort from the symptoms
If significant symptoms - may need to find alternative medication
Discuss with GP
What is the defintion of amalgam contact sensitivity LP?
Is it the amalgam, Mercury or something else as the trigger
Patch test to the allergen
How to manage an amalgam related lichen planus lesion?
If asymptomatic do nothing
Any replacement will lose tooth tissue
Which materials to replace amalgam with?
Composite
Glass
Gold - low palladium alloy
Bonded crown
Srmamentarium for amalgam removal?
Dam
High vol suction
PPI
Avoid during preg
Explain the overall lichen planus management for the patient?
Remove any cause
- medicines
- dental restorations
Biospy
- unless a good reason not to
Blood test
- haematinics
- fbc
- if lulus suspected autoantibody screen for ANA, Ro and dsDNA
What treatment would be recommended for mild intermittent lichen planus lessons?
Topical OTC remedies
- chlorhexidine
- benzdamine
Avoid SLS containing toothpaste
What treatment would be recommended for a persisting synthetic lichen planus lesion?
Topical steroids
- beclomethasone inhaler
- betamethasone rinse
Higher strength steroid
- skin steroid cream - Clobetasol
Topical tacrolimus mw
Hydroxycholorquine
Systemtic immumodilators
- azathioprine and mycophenolate
Graft vs host disease
What are the histological findings of lupus erythematosis?
Basal vacuolar damage
Atrophic epithelium
Melanophage
Intense lymphocytic infiltrate
Describe lichen like lesions?
Underlying disease needs consideration
GVHD common after stem cell transplant
Lupus lesion can be
- only in mouth - discoid lupus no auto abs
- mouth and elsewhere (systemic ANA/Ro/dsDNA
If oral symptoms only treat like lichen llanjs
Name 5 vesiculobulloua conditions?
Erythema multiform
Pemphigus
Pemphigoid
Angina Bullish Haemorrhagia
Bullous lichen planus
What is the defintion of Pemphigoid?
A subepithelial antibody attack
Thick walled blisters
- persist to be seen
- clear or blood filled
Name 3 different forms and presentations of Pemphigoid?
Bullous pemphigoid - skin
Mucous membrane pemphigoid - all mucous membranes
Cicatritial pemphigoid - mucosal with scarring
Describe the histopathogy of pemphigoid?
Sub epithelial split - epithelial/CT tissue junction
Hemi-desmosomes involved at basement membrane
Describe how Pemphigoid is seen with immunofluorescence?
Linear staining along the basement membrane
C3 and IgG detected in this area in ‘standard’ pemphigoid
IgA occasionally found
- linear staining with C3 is ‘Linear IgA disease’
- granular IgA and C3 deposits is seen in ‘dermatitis herpetiformis’
What is a symblepharon?
Pemphigoid that is present on the eye
Non-oral locations of Pemphigoid?
Oral and skin lesions
- bullous on skin
- mucous mem usually mouth, eye or genitals (needs specialist)
Scarring is a feature in some cases
- cicatritial pemphigoid
How to manage Pemphigoid?
Steroids
Immune modulating drugs
- azathioprine
- mycophenolate
What is the defintion of Pemphigus?
Commonest form is vulgaris
Intraepithelial bullae
Clinically:
- more common in females and over 50s
- genetic with ashkenazi Jews
Sites:
- skin
- mucosa
They blister, then burst and then it spreads
Describe Pemphigus histopathologically?
Supra-basal split with tzank cells
Describe Pemphigus using immunofluorescence?
Very green
Basket weave pattern - around each epithelial cell
C3 and IgG in Pemphigus vulgaris
How to treat Pemphigus?
It affects the mucosa and skin
Rarely see intact bullae
- intra epithelial blisters
Can be fatal without disease
- complications of treatment are major cause of death
Explain 2 different types of immune mediated disease?
Hypersensitivity
Immunogenic
How many types of hypersentivitiy?
5
Name the 2 types of immunogenic immune mediated disease?
Cell mediated
Antibody mediated
Name 3 types of local immunological oral disease?
Aphthous ulcers
Lichen planus
Orofaxial granulomatosis
Name 6 systemic diseases with local oral effects?
Eythema multiform
Pemphigus
Pemphigoid
Lupus
Systemic sclerosis
Sjogren’s syndrome
Type 3 Hypersensitivity example?
Erythema multiform
Name 3 examples of cell mediated immunity?
Aphtous ulcers
Lichen Planus
Orofaxial Granulomatosis
Name 2 examples of antibody mediated immunity?
Pemphigus
Pemphigoid
Immunological skin diseases?
Skin and oral.mucosa.share many antigens and epitopes
- blistering skin conditions can also affect the mouth
Explain the mechanism of immunological skin disease?
Auto-antibody attack on skin compartments causing loss of cell to cell adhesion
- causing splits in the skin
- fill with inflammatory exudate
- form vesicles or blisters
How do cells of the epidermis adhere to eachother?
Via desmosomes and hemidesmosomes
2 proteins - desmoglein (VIP) and desmocollin
Explain the mechanism of action for immunofluorescence?
A fluorescein molecule is attached to an engineered antibody, that when binds fluorescence and becomes active
Explain the difference between direct and indirect immunofluorescence?
Direct:
- antibody mediated tissue disease
- antibody bound to tissues - targeted in DIF
Indirect:
- circulating antibody not yet bound to the tissue
- detected by immunofluorescence from a plasma sample
- not always useful for diagnosis - often good for monitoring disease activity
What is the defintion of erythema multiforme?
Acute onset - more men
Skin - show target lesions
Mucosa - show ulcers
For young males it is recurrent within a short period
What is the aetiology of erythema multiforme?
Immune complex?
- drugs
- herpes simplex
- mycoplasma
What specific sites do erythema multiforme target?
Lips and anterior part of the mouth
Heals in 2 weeks
Very painful - unable to eat or drink
What os erythema multiforme relation to Stevens Johnson syndrome?
Can be involved with Stevens-Johnson syndrome
- sevre multisystem involvement
- skin, conjunctivae, nose, pharynx, mouth and genitals
What is the treatment for erythema multiforme?
Oral lesions:
Urgent medical therapy:
- systemic steroids of up to 60mg per day
- systemic aciclovir
Encourage fluid - possible I
Encourage analgesia
If recurrent:
- prophylactic acyclovir daily
- allergen test for triggers
Mycoplasma infective agent
What is the defintion of angina bullous haemorrhagica?
Commonest oral blistering condition
Blood blisters in mouth:
- buccal mucosa and soft palate
- rapid onset
- 1 hr then burst
Painless
Iniated by minor trauma or eating
Heal with no scar within days
Give a brief overview of how to treat and what tests for angina bullish haemorrhagica?
Non specific ulceration
DIF and IFF negative
No defects
Chlorhex MW
May recur
How to manage angina bullish haemorrhagica?
No treatment
Reassure patient that is benign
Explain known triggers
Why are mucosal lesions more frequent in children?
Clinical issues traditionally related to immunological
immaturity
Name the 2 types of congenital oral mucosal lesions?
Hereditary
Developmental defects
Name the 6 types of acquired oral mucosal lesions?
Traumatic
Drug-related
Chronic inflammatory
Hyperplastic
Neoplastic
Infective
What is the defintion of white sponge naevus?
Hereditary
Inherited as autosomal dominant condition . Defect in keratin gene 4 and 13.
Uncommon
Name the clinical features of white sponge naevus?
•White, soft, irregularly thickened, no
defined borders
•Bilateral
•Genital tissues can also be affected
•Often misdiagnosed with candidosis
Name the histopathology of white sponge naevus?
•Uniform acanthosis
•Hyperparakeratosis
• Intracellular oedema
•No dysplasia, no inflammation
How to manage white sponge naevus?
Reassurance
Name 3 developmental defect oral mucosal lesions?
Fordyxe’s granules
Foliate papillae
Geographic tongue
Describe the clinical features of fordyce’s granules?
▪Ectopic sebaceous glands
▪Association with hormonal changes in puberty?
▪Bilateral, most commonly on buccal mucosa
Describe the clinical feattures of folaite papillae?
▪Pinkish soft nodules
▪Bilateral, ventral tongue
▪Lymphoid tissue, sometimes
inflamed/hyperplastic
Describe the clinical features of geographic tongue?
▪Dorsum of tongue
▪Irregular, smooth, red areas (depapillated)
with sharply-defined edge
▪Recurrent, migrates
Describe the histology of geographic tongue?
▪Thinning of epithelium at centre, mild
hyperplasia at periphery
▪Epithelium infiltrated by neutrophils
Explain how to manage geographic tongue?
reassurance. If symptomatic exclude heamatological deficiencies.
Median rhomboid glossitis generally not seen in children
Name 3 traumatic oral mucosal lesions?
mucocele
traumatic ulcer
frictional keratosis
Describe the clinical fearues of frictional keratosis?
▪Pale and translucent or white/dense with
rough surface
Describe the histology of frictional keratosis?
Epithelial hyperplasia, with thick granular
cell layer and hyperorthokeratosis
▪Scattered subepithelial lymphocytes
Describe the clinical features of traumatic ulcer?
Mechanical, thermal or chemical trauma
▪Inflammation levels and clinical features vary
▪Yellowish floor of fibrin slough often present
Describe the histology of traumatic ulcers?
Non-specific ulceration. See RAS
▪Destruction of epithelium
▪Tissue infiltration by neutrophils
Describe the clinical features of a mucocele?
▪Most commonly on lower labial mucosa
▪Overlying mucosa is intact and healthy
typically circular
▪Firm or fluctuant and bluish
Describe the histology of a mucocele?
▪Damage to duct of salivary gland
▪Mucin and macrophages surrounded by
compressed connective tissues
▪No epithelial lining
Name a drug-induced oral mucsoal lesion?
Chemo-induced stomatitis
Aspirin burns
Name 3 types of inflammaotry oral mucosal lesions?
Orofacial granulomatosis
erythema multiforme
recurrent apthous stomatitis
Describe the clinical features for recurrent aphthous stomatitis?
▪Idiopathic, but systemic factors known to modulate the severity of disease
▪Onset in childhood, but peak in adolescence
Minor
Major
Herptiform
Describe the histology of recurrent aphthous stomatitis?
▪Initial lymphocitic infiltration?
▪Destruction of epithelium
▪Tissue infiltration by neutrophils
▪Dilated vessels
Explain the management for a mucocele?
Reassurance/excision if symptomatic or interferes with oral functions
What should be excluded when dealing with recurrent aphthous stomatitis?
Extraoral involvement should be excluded, e.g. GI (coeliac disease, Crohn’s), genital/ocular
(Behcet’s).
Describe the clinical features for erythema multiforme?
▪Mostly HSV-related, drug-induced
▪Cutaneous erythema or “target” lesions
▪Ulceration of outer lip with bleeding,
crusting.
▪Intraorally irregular fibrin- covered erosion
and erythema
▪Ddx with HSV-1 infection
Describe the histology of erythema multiforme?
▪Necrosis of keratonocytes
▪Epithelial infiltration by inflammatory cells
▪Intraepithelial or subepithelial vesiculation
Describe the clinical features for orofacial granulomatosis?
▪Swelling of the lips
▪Mucosal nodularity (cobblestoning)
▪Mucosal tags
▪Gingival hyperplasia
▪Aphthous oral ulcers
▪Children more likely to develop Crohn’s disease
Describe the histology for orofacial granulomatosis?
Granulomas containing
multinucleated giant cells
▪Lymphoedema
What are possible differential for orofacial granulomatosis?
DDx with sarcoidosis and tubercolosis. Primary TB of the oral cavity is rare,?more
common in children than adults
Name 3 inflammaotry oro mucosal diseases rarely seen in children?
Oral Lichen Planus
• Mucous Membrane Pemphigoid
• Pemphigus vulgaris
Describe the clinical features for oral lichen planus?
▪White striae and/or mucosal atrophy, and/or
erosions, and/or plaques
▪Desquamative gingivitis in isolation or in
combination with above
▪Bilateral lesions
Describe the histology for oral lichen planus?
Basal membrane thickening
Band-like lymphocitic infiltrate
Colloid bodies,
apoptotic basal cells
Describe the clinical features for mucous membrane pemphigoid?
▪Bullae, sometimes intact, can appear as blood
blisters. If ruptured raw ulcer
▪Desquamative gingivitis
▪Conjuctival involvement
▪Cutaneous involvement less prominent than
bullous pemphigoid
Describe the histology for mucous membrane pemphigoid?
•Separation of full thickness of epithelium from CT
•Linear deposition of IgG and C3/C4 along basal
membrane.
•Auto-antibodies bind along basal membrane indirect immunofluorescence assay
•CT infiltrated with inflammatory cells
Describe the clinical features of pemphigus?
▪Fragile vesicles/bullae
▪Ruptured vesicles
▪Nikolsky’s sign positive
▪Widespread cutaneous involvement
Describe the histology for pemphigus?
•Acantholysis
•Intraepithelial vesicles.
•‘Chickenwire’ deposition of IgG and C3/C4
within the epithelium.
•Anti-desmoglein3 antibodies bind
intercellular substance in direct
immunofluorescence assay
Deswcribe the clinical features for epydermolysis bullosa?
▪Subepithelial bullae leading to severe scarring after minimal trauma.
▪Type VII collagen defect.
▪Autosomal recessive
Name 3 hyperplastic forms of oral mucosal lesions?
Vascular malformation
Giant cell epulis
Pyognic granuloma
Describe the clinical features for a pyogenic granuloma?
▪Soft, red polypoid
swelling
▪Most commonly gingival
but not exclusively
Describe the histology for a pyogenic granuloma?
•Granulation tissue
•Dilated blood vessels in
oedematous CT
•Dense infiltration by
neutrophils
NO GRANULOMAS, NO
PYOGENIC BACTERIA
Describe the clinical features of a giant cell epulis?
▪Soft, violaceus swelling
▪Central gingival segments
Related to resorption of deciduous teeth?
Describe the histology for giant cell epulis?
•Subepithelial clusters of giant cells in fibro-
vascular tissue
What to exclude when dealing with a giant cell epulis?
Need to exclude central GCG and
underlying hyperparathyroidism
Describe the clinical features of vascular malformation?
Purple nodular lesion
▪Blanches upon pressure
Describe the histology for a vascular malformation?
•Capillary: small vessels and vasoformative tissue
•Cavernous: large blood filled sinusoids
Name 2 pigmentary chnages ivolved with oral mucosal lesions?
Puetz-Jeghers syndrome
Addison’s Disease
Name the clinical features of Peutz-Jegher’s syndrome?
Clinical features
▪Intestinal polyposis
▪Mucocutaneous pigmented lesions
appearing during childhood
Describe the histology for Addison’s disease?
•Mild acanthosis
•Melanin in basal layer
Describe the clinical features for warts?
HPV 2, 4
•White or pinkish, raised
•Sessile or pedunculated
•Often multiple
•Mainly secondary to self inoculation
Describe the histopathology of warts?
•Papillary processes of hyperplastic epithelium with acanthosis, hyperkeratosis,
hyperplastic basal cell layer
•Connective tissue core
•Koilocytes often present
Describe the clinical features for pseudomembranous candidosis?
•Acute
•Thick white pseudomembranes of various sizes
•Erythematous background
•Often idespread
Diseases that cause immunocompromisation and lead to oral mucosal lesions?
HIV/AIDS
How are viruses transmitted?
Exchange of blood products
Sexual transmission
Perinatal infection
MoA of HIV?
Retrovirus - group VI (baltimore)
Infects activated T cells and macrophages vis the envelope glycoprotein
Transferred by dendritic cells via DC-SIGN, then migrate to lymph nodes to transfer the CD4 T cells
How does HIV infect T cells?
HIV gp120 binds T cells through CCR5/CXCR4 and CD4
How does HIV infect macrophages?
HIV gp120 binds macrophages through CCR5 and CD4
What infections are diagnostic for acute HIV infection?
Pyrexia
Skin rash
Haedache
Diarrhoea
Oropharyngitis
Oral mucosal erythema
What infections are diagnostic fir ARC asymptomatic seropostive HIV?
Lymphoadenopathy
Persistent pyrexia
Diahorrea
Weight los
Fatigue and malaise
What infections are diagnostic for AIDS?
Kaposi’s sarcoma
NH lymphoma
Thrombocytopenia
Neurologival diseases
What drug is Pre-exposure prophylaxis of HIV?
Trivada - emtricitabine
When will HIV/AIDS related oral lesions occur?
May occur during mild immunodeficiency and prior to severe opportunistic infections
Evidence suggests that patient s with oral.lesikns may progress to AIDS more rapidly compared to patients without
Why can oral lesions occur?
Immunodeficiency
Name 5 oral mucosal lesions strongly associated with HIV?
Candidiasis: - erythematous, pseudo and angular cheilitis
Hairy leukoplakia
Kaposi sarcoma
NH lymphoma
Perio disease: linear gingival erythema, necrotising gingivitis and periodontitis
- more commonly seen due to immunosuppressant therapy
Describe candidiasis in HIV patients?
Mild immunodeficiency
If psuedomem, indicative of acture immunosuppression
- widespread oropharyn and oesoph
Can persist for month
Erythamtous
Hyperplastic
Describe linear gingival erythema in HIV patients?
Red band involving the free gingival margin - not plaque induced
- hypermedia due to vasoactive cytokines
Describe hairy leukoplakia in HIV?
Not pre malignant
White patches that can’t be removed
Lateral border of the tongue
Vertical white folds with hair like surface
Smooth
Describe the histopathology of hairy leukoplakia?
Acabthotic parakerarinsed epithelium
Finger like keratin projections on the surface
Band of ballon cells in prickle cell layer
Secondary candidal infections
Swollen cells are EBV+ (koliocytes), EBV demonstration essential for diagnosis
Describe Kaposi sarcoma in HIV patients?
Most commonly associated with HIV
HHV8
Involves skin and mucosal surfaces
Red purple patch - becomes nodular
Describe the histopathology of Kaposi sarcoma?
Early lesions consit of proliferating endothelial cells, extravasated blood cells, haemosiderin and inflamm cells
Late lesions have a more predominant vascular component and atypical spindle cells
Describe non-hodgkins lymphoma in HIV patients?
AIDA and severely immunocompromised patients
Associated with EBV
Name 4 less commonly oral mucosal lesions with HIV?
Bacterial infections
Salivary glabd disease
Oral ulceration
Viral infections
Describe HSV and VZV infections in HIV?
More severe and higher recurrence
Describe the HPV infection in HIV patients?
6,11 and 16
Venereal war
Transmitted via oro genital contact
Multiple white/pink nodules
Fuse forming sessile or pedunculated papillary lesions
Describe the histopathology of HPV in HIV patients?
Induce hyperplastic changes rather than ballooning degeneration
Fibrovascular core covered by stratified squamous epithelium with
- hyperpladtiv basal cell layer
- acanthosis
- parakeratosis
Koilocytes
Describe atylical ulceration in HIV patients?
Oropharyns most commonly affected
Associated with CMV infection
- can also be aphthous stomatitis
Describe salivary gland disease in HIV patients?
Salivary gland enlargement - mainly parotid
Xerostomua
Lymphocyte infiltration
Lympho-epothelial cysts
Enlargement of intraparotid nodes as part of P
How is Oral cancer classified?
International Classification of Disease for Oncology
- ICD-O
What makes classification of cancer difficult?
Makes comparison difficult
Makes epidemiology difficult
Makes treatment planning difficult
Name the 2 distinct disease patterns for oral cancer?
Oral Cavity Cancer (OCC)
Oro-Pharyngeal Cancer (OPC)
Describe the epidemiology of OCC?
2.5 per 100,000 pop (2012)
Almost HALF (48.7%) in south central Asia
Male 2:1 Female
Incidence not increasing worldwide
- Decreasing in men, increasing in women
- Linked to reduction in tobacco use
Scottish Cancer Registry
- 10% increase 2001-2012
Name the 6 common sites for mouth cancer?
Floor of the mouth
Lateral border of the tongue
Retromolar regions
Soft and hard palate
Gingivae
Buccal mucosa
Name the 3 higher sites for SSC in drinkers and smokers?
FoM
Lat. border of the tongue
Soft palate
Name the 8 sites of oral cancer?
Lips
Palate
Tonsils
FoM
Other throat
Tongue
Oropharynx
Gums
Describe the epidemiology for OPC?
1.4 per 100,000 pop
Most in North America and south central Asia
Male 4.8:1 Female
Rates rapidly rising, especially in High Income areas (North America)
- Linked to rising HPV epidemic
Scottish Cancer Registry
- 85% increase 2001-2012 – highest increase for any cancer
Name the 5 main risk factors and their associations to Oral Cancer? - how much does each RF multiply the risk of OC?
Smokers who don’t drink x2 risk
- Increases with quantity, duration and frequency of tobacco use
- Fewer cigarettes for longer duration worse than high number, short term
- Smoking risks were generally greater for larynx cancer
Drinkers (3-4 drinks/day) x2 risk
- Never smoked population
- Frequency more important than duration – more drinks each day key
- alcohol drinking for oral cavity and pharyngeal cancers
Smoke and Drink x5 risk
- Increases with frequency and duration of smoking and alcohol consumption
- No safe lower limit
Betel quid (paan) x3 risk
- mixture of substances including areca nut with or without tobacco wrapped in a betel leaf and placed in the mouth
Socioeconomic Status x2 risk
- Even without other risk factors
- Low educational attainment
Name the 3 risk factors that have not been confirmed as certain to increase the overall risk of Oral cancer?
Family History
- 1st degree relative with H&N cancer may be important
Oral Health
- Early data suggests poor oral health may be associated with an increased cancer risk – small effect
Sexual Activity
- a slight increased risk for oropharyngeal cancer with:
- six or more lifetime sexual partners
- four or more lifetime oral sex partners
- early age (<18 years) of sexual debut (INHANCE)
What are the benefits of reducing smoking and alcohol intake?
Benefits seen between 1-4 years
Risks reduced and reached a similar level to those who had never smoked after 20 years of quitting.
In contrast, the risk effects associated with quitting heavy alcohol consumption take 20 years to begin to emerge.
What are the benefits of improving SE status?
Socioeconomic status
- SE status is on a par with smoking and alcohol in terms of magnitude (two-fold increased risk)
- specifically low educational attainment and low income.
- These risks were not fully explained by smoking and alcohol consumption (‘the cause of the cause’)
- have a more direct effect associated with socioeconomic circumstances
What are the benefits of reducing poor diet choices?
- There is limited new evidence in relation to dietary factors beyond confirming that a high intake of fresh fruits and vegetables were associated with reducing by half the oral cancer risk
- Obesity was not associated with an increased oral cancer risk
- young people (aged 30-years or less) oral cancer was more likely in those who self-reported a low body mass index (BMI)
Name 4 potentially malignant lesions?
White lesions (leukoplakia)
Red lesions (erythroplakia)
Lichen planus
- Candidal Leukoplakia
- Chronic Hyperplastic Candidiasis
Oral Submucous Fibrosis
Describe the epidemiology of white lesions in OC?
incidence 0.2 - 4%
- wide variation in different populations
- Reliability of data not clear
malignant change
- varied reports, most under 4%
- period prevalence
2.5% in 10 years, 4% in 20 years
Most oral carcinomas in UK arise in initially clinically normal mucosa
Most cancer in high incidence areas (e.g. India) from potentially malignant lesion
Worldwide leukoplakia is 50 to 100 times more likely to progress to cancer than clinically normal mucosa
Name 3 types of descriptions of white lesions?
Homogenous
Erosive
Non-homogenous on atrophic background
How does erythroplakia compare to leukoplakia?
much less frequent than leukoplakia
much higher risk of cancer
greater dysplasia risk
- Up to 50% already be carcinoma
no good follow-up studies available
What are the common characteristics of dysplasia and the new categorisation of severity?
Based on:
- Cellular Atypia
- Epithelial Architectural Organisation
New categorisation
- Low grade
- high grade
- carcinoma-in-situ
Describe the histological low grade of oral mucosal dysplasia?
Easy to identify that the tumour originates from squamous epithelium
Architectural change into lower third
Cytological atypia or dysplasia may not be prominent
Shows a considerable amount of keratin production
Evidence of stratification
Well formed basal cell layer surrounding the tumour islands
Tumour islands are usually well defined and are often continuous with the surface epithelium
Invasion pattern with intact large branching rete pegs ‘pushing’ into underlying CT
(Where there is architectural change into middle third, depending on the level of cytological atypia will be classified into low grade or high grade)
Describe the histological high grade of oral mucosal dysplasia?
Show little resemblance to a normal squamous epithelium
Architectural change upper third
Usually show considerable atypia
Invade in a non-cohesive pattern with fine cords, small islands and single cells infiltrating widely through the CT
Mitotic figures are prominent and many may be abnormal
Degree of differentiation used to predict prognosis
Describe the histological carcinoma in situ of oral mucosal dysplasia?
Theoretical concept
Cytologically malignant but not invading
Abnormal architecture
- Full thickness (or almost full)
- Severe cytological atypia
Mitotic abnormalities frequent
Name the histoloigcal prognostic facors which give information on survivability?
Pattern of Invasion
- Bulbous rete pegs infiltrating at same level is considered of a better prognosis than widely infiltrating small islands and single cells
Depth of Invasion
- Risk of metastases for a tumours greater than 4mm was 4x greater than for a tumour less than 4mmm
Perineural Invasion
- Is seen in up to 60% of OSCCs but is most significant when a tumour is seen within a large nerve at a site some distance from the main tumour mass
Invasion of Vessels
- Widely thought to be associated with lymph node metastaes and a poor prognosis
Describe the Field Cancerisation concept?
Multiple primaries possible over time
- up to 15 to 20 in some patients
Concept of “field cancerisation”
- high cancer risk in 5cm radius of original primary - that’s most of the mouth/pharynx
Synchronous or metachronous lesions
- Can occur at the same time as the primary or at later times
Name the multiple variables for clinical cancer staging of OC?
site
size (T)
spread (N&M)
Describe the different varying change of cancer prognosis/survivability?
1/3 patients present at stage I/II
- Stage I - 80% cure rate
- Stage II – 65% cure rate
- Later than this 5 year survival <50%, cure <30%
- If untreated, with metastases, survival is about 4 months
Surgery, Radiotherapy and Chemo/Immunotherapy all used
- Choice will depend on patient choice and health/prognosis
- Tumour location, size and nutitional status all important
For resectable tumours, primary surgery offers the best outcome
- Post surgical radiotherapy or chemotherapy
Describe the aetiology, behaviour and prognosis of Lip cancer?
Lower lip
- non-healing ulcer or swelling
Aetiology
- Sunlight UV-B
- smoking
Behaviour
- slow growth
- local invasion
- rarely metastasise to nodes
Good prognosis as early detection
How is OC detected?
Difficult to do – a judgement from experience
- Use the ‘Oral Cancer Recognition Toolkit’
- Developed jointly by Cancer Research UK and the British Dental Association
What are the advantages and disadvantages of OC screening?
Benefits vs Harm
Undetected lesions vs False positive
Cost of Screening vs Cost of disease
Cost of Screening vs Disability from disease
Name the 5 OC screening tools?
HPV16 screening
Toluidene blue
VELscope
Photodynamic Diagnosis (PDD)
Clinical judgement of experienced clinician
Describe what and how toluidine blue is and used?
false positive in inflammatory lesions
? 50 % false negatives
good for invasive disease, but usually clinically evident
Describe what and how VELscope is and used?
Autofluorescence of tissues with blue light
- Loss of fluorescence equates to ‘change’
- Change may be cancer but can be other changes
Published work ‘thin’
- May well work, but evidence not yet adequate
Explain the duty of Primary care dentistry in OC screening/detection?
Part of General CPD requirement now
Dentist has opportunity for PRIMARY PREVENTION in patients attending for regular oral care
Dentist must be familiar with and competent in:
- Smoking cessation advice
- Alcohol reduction advice
- Healthy diet promotion
There is a GDC expectation that a dentist will do this as part of ‘good patient care’ rather than any particular remuneration
Dentist has to make decision about their referral threshold for potentially malignant lesions
Monitor with photographs and education
Remove local factors where ulcer may be due to trauma, then review
2 WEEK RULE for referral to clinic for the hospital
Patient must be initially seen within this time
62 day referral to treatment time for cancer patients
What is the definition of precancerous lesion?
An altered tissue in which cancer is more likely to form
What is the defintiion of precancerous condition?
A generalised state associated with an increased cancer risk
Name the 4 types that can’t be conisdered leukoplakia?
Tobacco related lesions
Smokers keratosis
Chronic hyperplastic candidosis
Frictional keratosis
What is the definition of leukoplakia?
It is a clinical diagnosis
It has NO histological connotation
Epithelial dysplasia may or may not be present
Non-homogeneous types are more likely to be dysplastic
Describe the epidemiology of leukoplakia?
- Incidence ? 0.2 – 10% but wide variation in different parts of the world. 6 x commoner in tobacco users. Male > Female world wide but only marginally so in the west. More common in the “elderly.”
- Malignant change in 3 -28%
- Period prevalence - how many in what time?
2.5% in 10 years, 4% in 20 years (West)
? % in Far east and Africa
Name the clinical predictors of malignancy?
Clinical appearance - very variable
Non-homogeneous
Verrucous, speckled,
Ulcerated, leuko-erythroplakia
Describe the molecular progression of oral cancer?
The development of oral cancer involves the progressive accumulation of 6 -10 genetic alterations in an epithelial cell leading to uncontrolled proliferation and clonal expansion.
A genetic progression model based on chromosomes frequently identified as showing Loss of Heterozygosity (LOH) in oral carcinogenesis suggests:
- Normal mucosa experiences a LOH at 9p: leads to predysplastic lesion.
- Predysplastic lesion experiences an additional LOH at 3p, 17p :leads to dysplasia.
- Dysplastic lesion experiences further LOH at 11q,13q and 14q leads to carcinoma-in-situ.
- C-I-S lesion experiences a further LOH at 6p,8,4q which leads to invasion
What is the definition of hyperplasia?
Increased cell numbers
Architecture
regular stratification
altered compartment size
NO cellular atypia
What is the definition of hyperplasia?
Increased cell numbers
Architecture
regular stratification
altered compartment size
NO cellular atypia
What is the definition of hyperplasia of stratum spinosum (acanthosis)
Architecture -
increased
maturation
compartment
What is the definition of basal cell hyperplasia?
increased basal
cells
What is the definition of low grade (mild hyperplasia)
Architecture -
change in lower third
Mild -
cytological atypia
What is the definition of high grade (mod/severe dysplasia)
Architecture -
change into
middle/upper third
Marked cytological
atypia
Possibility of numerous abnormal mitoses
What is the definition of oral candidosis?
Opportunistic fungal infection of the oral cavity.
- Oral rarely in itself painful
- Oesophageal may be in HIV
How do people aquire candida?
Majority of normal population are healthy carriers
Most common isolate is C. albicans
Name 5 candidal virulence factors?
Adherence
Switching mechanisms
Germ tube formation
Extracellular enzymes
Acidic metabolites
Name the local predisposing factors for candidal infections?
Smoking
Dentures
Local corticosteroids
Xerostomia
Topical antimicrobials
Name the general predisposing factors for candidal infections?
Extremes of age
Endocrine disease
- Diabetes
Immunodeficiency
- Steroid use, HIV
Nutritional deficiency
- iron
Antibiotics
Name the classification of oral candidosis?
Acute Pseudomembranous
- Sudden local/systemic immunosuppression
Chronic Erythematous
- Longstanding & persisting issue
- e.g. below poor fitting dentures, HIV, median rhomboid glossitis and antibiotic
Chronic Hyperplastic
How to diagnose oral candidosis?
Laboratory tests
- Differentiate from commensal
- Only by QUANTIFIABLE assay
- Culture and sensitivity to inform treatment
- Multiple sites usually
- Smear/microscopy occasionally
How to diagnose candidosis via lab?
Swab (mucosa or denture )
Whole saliva/Oral rinse
- Growth onto selective agar
Oral rinse
- Patient rinses with 10ml of PBS. Inoculate onto selective agar on spiral plater.
- Has the advantage of being a “Quantitative technique”
How to identify candidaosis in the lab?
Direct microscopy
Germ Tube test
Physiological tests
- Carbohydrate fermentation
- Carbohydrate and nitrogen assimilation
Commercial systems
- API 20C systems
How to identify candidaosis in the lab?
Direct microscopy
Germ Tube test
Physiological tests
- Carbohydrate fermentation
- Carbohydrate and nitrogen assimilation
Commercial systems
- API 20C systems
Biopsy
- Essential for diagnosis of hyperplastic candidosis.
- PAS stain
Direct smear
Name the 5 candida species?
C. albicans
C. glabrata
C. tropicalis
C. krusei
C. dubliniensis
Describe the principles of management for candidal infection?
Correction of predisposing factors
OH, diet, trauma, steroid inhaler hygiene
Identify underlying illnesses
Antifungal agent
Co-infection with other microorganisms?
Name different categories of antifingal drugs?
Polyenes
- Nystatin
- Amphotericin
Imidazole
- Miconazole
- Clotrimazole
Triazoles
- Fluconazole
- Itraconazole
Explain the treatment regimes for oral candidosis?
Topical Therapy (lengthy courses required)
- Nystatin (pastille, suspension, cream and ointment)
- Amphotericin (not available in the UK)
- Miconazole
Systemic treatment (often preferred)
- Fluconazole
- Itraconazole
What is the definition of miconazole?
- Imidazole antifungal
- Not absorbed systemically
- Available as a cream, ointment, patch or a gel
- Don’t use gel for skin lesions (orange!)
- Cream/ointment available with hydrocortisone
- Available without prescription
Slow release adhesive preparation available
ACTIVE AGAINST STAPHYLOCOCCI as well as Candida
Name the types of systemic antifungals and their treatment regimes?
Fluconazole
- 50mg capsules taken once daily
- 14 day course
Itraconazole
- 100mg capsule
- 14 day course
- 100mg twice in once daily for Pseudomembranous candidiasis
Name 3 antifungals that have resistance?
C. glabrata
C. kruseii
C. dubliniensis
Name the disease that come from Human herpesvirus/
Herpes simplex virus (HSV)
- Primary herpetic stomatitis
- Herpes labialis (recurrence)
Varicella-Zoster Virus (VZV)
- Chickenpox
- Zoster (recurrence)
Epstein-Barr Virus
- Infectious mononucleosis
Cytomegalovirus (CMV)
HHV8
- Kaposi’s sarcoma
Explain the virion replication cycle?
Virus attachment and entry
Uncoating of virion
Migration of acid to nucleus
Transcription
Genome replication
Translation of virus mRNAs
Virion assembly
Release of new virus particles
Effect of viral infections on host cells?
Cell death (cytopathic effect)
Latent infection
Hyperplasia
Transformation
Explain the lifecycle of HSV, VZV associated leison?
Intranuclear oedema (glass-appearance of nuclei) at basal cell layer
“Ballooning degeneration” : Keratinocytes swelling and loss of attachment. Cells can be multinucleated with eosinophilic intranuclear inclusions and eosinophilic cytoplasm
Progressive cell swelling (cells are large and clear)
Rupture of infected cells and release of viral particles to non-infected cells
Explain how to diagnose human herpesvirus?
Laboratory investigations available:
- Antigen-specific IgG or IgM serum titres
- PCR
- Immunofluorescence, immunocytochemistry on affected tissue
- Virus isolation from lesion and cultivation
Describe the apperance of primary herpetic stomatosis?
HSV-1
- Incubation period: 5-7 days
- Intraoral vesicles
- Vesicles on lips and crusting due to exudate coagulation
- Generalized gingival inflammation
Extra-oral involvement:
- peri-oral
- fingers (herpetic whitlow)
- eyes
Symptoms
- Pain
- Dysphagia
- Dehydration
- May be associated with fever, lymphadenopathy,
- Pharyngitis in adolescents
Recurrent infection:
- Occur in the same location, unilateral and recur 2-3 times a year on average
- Most commonly on lips, but can involve other perioral tissues
- Erythematous areas papules vesicles ulcers
- Intraoral mucosal involvement is less common.
- Chronic ulcers in immunocompromised individuals
Describe the apperance of chickenpox and recurrent zoster infection
VZV
- Prodromes: fever, fatigue, pharyngitis
- Small ulcers (rarely intact vesicles) mainly on soft palate and fauces
- Intraoral lesions may precede skin lesions
Recurrent infeection (Zoster)
- Prodromes: pain and parasthesia
- Unilateral vesicular eruption following distribution of sensory nerves, e.g. divisions of the trigeminal nerve, geniculate ganglion of facial nerve (Ramsay Hunt syndrome).
- Intraoral vesicles rupture quickly
- Cutaneous lesions clear within 3 weeks. Pain may persist (post-herpetic neuralgia)
Describe the managment for HSV-1 and VZV mild infections?
Symptomatic relief :
- Hydration
- Rest
- Pain relief
- Antimicrobial mouthwashes (chlorhexidine 0.2%, H2O2 6%)
Mild infection of the lips in healthy individuals:
- Aciclovir cream 5% every 4 h
- Penciclovir cream 1% every 2 h
Describe the managment for HSV-1 and VZV severe and immunocompromised infections?
Severe infections in non-immunocompromised patients:
- 200 mg Aciclovir tabs or oral suspension, 5 times daily, 5 days
- Prophylaxis: aciclovir 400mg twice daily (in liaison with specialist)
Immunocompromised patients:
- 400mg Aciclovir tabs or oral suspension, 5 times daily, 5 days
- Both adults and children
Immunocompromised with severe infection:
- Refer to specialist/GP for treatment
Shingles:
- 800mg Aciclovir tabs or oral suspension, 5 times daily, 5 days, within 72 h onset of rash
- Not in children
- Refer to specialist/GP
Describe the apperance of infectious mononucleosis?
EBV:
- Long incubation period (4-6 weeks)
- Prodromes: severe fatigue, malaise and anorexia (10-15 days)
- Main symptoms: fever, pharyngitis and generalized
lymphoadenopathy (cervical nodes)
Diagnostic features:
- Paul-Brunell test +
- Raised anti-EBV antibodies.
- If above are negative consider CMV and toxoplasmosis.
- Possible oral signs: tonsilar exudate, palatal petechiae
Describe the apperance of CMV?
Mostly subclinical
If symptomatic, clinically similar to infectious mononucleosis
Large, shallow ulcers (Cytomegalovirus-associated ulceration) in immunocompromised individuals.
Histopathology: Non-specific ulceration but CMV+ inclusion bodies present at ulcer floor.
Describe the apperance of hand-foot and mouth disease?
Coxsackie Virus (A):
- Incubation period is 4-7 days. Highly infectious.
- Small ulcers (rarely intact vesicles) causing little pain mainly on buccal, labial, lingual and palatal mucosae
- Vesicles and ulcers on hands and feet (occasionally oral ulcers or skin rash in isolation)
- No gingivitis, no lymphadenopathy, no systemic upset
- Self-limiting (7 days)
Describe the apperance of herpangina?
Coxsackie A and B strains:
- Prodromes: muscular pain, nausea, malaise.
- Small ulcers mainly on palate, uvula, tonsils
- Associated with fever, dysphagia and oropharyngitis
- Self-limiting (8-10 days)
Describe the apperance of measles?
Koplik’s spots - Prodrome of measles (2-4 days before measles cutaneous rash).
Appear mostly on buccal mucosa (opposite molars).
White spots against an erythematous background.
Describe the apperance of warts?
HPV 2,4:
- White or pinkish, raised but mostly sessile
- Similar to squamous cell papilloma, but more rounded and sessile
- Often multiple
- Mainly children affected, secondary to self inoculation
Describe the apperance of squamous papilloma?
More common in individuals >20 of age
Exophitic, peduncolated
Distinctive branched structure, finger-like processes, white or pinkish
Up to 20 mm in diameter
Describe the apperance of condyloma acuminatum?
HPV 6, 11, 16:
Venereal wart
HIV infection manifestation
Transmitted via oro-genital contact
Multiple white/pink nodules.
Fuse forming sessile or pedunculated papillary lesion.
Describe the management of oral mucosal HPV-related lesions?
Diagnosis
- Clinical
- Biopsy (excisional if possible)
Treatment
- Reassurance and monitoring
- Cryotherapy
- Surgical excision
Describe the histopathology of oral mucosal HPV-related lesions?
HPVs induce hyperplastic changes rather than “ballooning degeneration”
Fibro-vascular core covered by stratified squamous epithelium with
- hyperplastic basal cell layer
- acanthosis
- hyperortho/parakeratosis
Koilocytes
Name the 2 categories for diagnosis of infections? And their options?
Clinical features
- history
- exam
Laboratory tests
- microscopy
- culture
- mass spec
- nucleic acid amp
- immuno tests
Describe what sampling and testing involves?
Culture and sensitivity:
- swab - mouth and related sites
Whole saliva
Aspirate
Smear
Biopsy
Blood
How to decide if infection need treatment?
Active symptoms:
- directly related to the infectious agent
Consequences of infection:
- local
- systemic
How to decide appropriate treatment for infection?
Culture and sensitivity test
- always preferred
Best guess
Experience
Side effect profile
Cost
What is the defintion of staphylococcal infection
Uncommon as an acute problem- immunocompromised
Very common as chronic mixed infection (related angular cheilitis)
Topical treatment sufficient
If systemic indicated- consider narrow spectrum
What is the defintion of scarlet fever?
Exotoxin mediated mucocutaneous manifestations
Name the 4 clinical features of scarlet fever?
Incubation period of 2-4 days
Prodromes: nausea, malaise, vomiting, pharyngitis and lymphoadenopathy
Macular erythema
Oral mucosa erythematous and oedematous
Dorsum tongue covered by white thick coating with enlarged fungiform papillae
What are the clinical features of tuberculosis?
Chronic, painless and irregular ulcer
Covered by yellowish exudate
Surrounding tissue indurated with inflamm
Localisation- tongue, palate gingivae, and lips
Assoc subman and services lymphoadenopathy
What isnthe histopathology of tuberculosis ?
Granukomas containing muktinuc giant cells
- mycobacteria not always identifiable
What are the oral manifestations of syphilis?
Primary - chancre
Secondary - mucosal patches and blisters
Latent
Tertiary - gumma, CV and CNS complications
What is the defintion of gonorrhea?
Second most common STI
Oral lesions result of progenitor contact
Non-specific oral presentation:
- multiple ulcers
- erythema
- white pseudomembranes
- painful pharyngitis
- lymphoadeno
What are the clinical features of actinomycosis?
Cerviofacial most common form
Painful and slow growing hard swelling
Absfesses and draining sinuses
Discharge yellow purulent material
What are the histopathologucal features of actinomycosis?
Colony of actinomyces in centre
Dense collection of inflamm cells
Surround by wall of fibrous tissue
What is the definition of sicca syndrome?
Partial Sjögrens findings
What is the definition of primary and secondary sjogrens syndrome?
Primary
- no connective tissue disease
Secondary
- connective tissue disease
- SLE, Rheumatoid Arthritis, Scleroderma
Name 4 types of auto-immune disease related to sjogrens?
Describe the background of Sjogrens Syndrome - spread? gender? systemic? genetic? environemnt?
0.2-1.2% (0.5-3 million in the USA) people have this
- Half ALSO have another connective tissue disease
Mostly women – 10:1
- Diagnostic delay due to late presentations
- Lifespan not affected
- Risk of neonatal lupus in baby if pregnancy
Systemic involvement
- Lungs, kidney, liver, pancreas, blood vessels, nervous system
- Sometimes general fatigue and chronic pain
Speculative Genetic
- Genetic predisposition – runs in families, but no specific inheritance
- Association with anti-Ro and anti-La seems genetic
- low oestrogen risk gives a of getting CT disease – androgens protective?
- Incomplete cell apoptosis leads to antigens being improperly exposed
- Dysregulation of inflammatory process with dendritic AP cells recruiting Band T cell responses and pro-inflammatory cytokines
Speculative Environment
- EBV association – weak evidence – may be reactive rather than causative
Describe the timeline of Sjorgens Syndrome
Name the 4 consequences of Sjogrens Syndrome?
Gradual loss of salivary/lacrimal gland tissue through inflammatory destruction
Enlargement of major salivary glands – usually symmetrical
- Usually painless
Increased risk
- Any lymphoma (5% quoted)
- Salivary marginal B-cell (MALT) Lymphoma
Oral and Ocular effects of loss of saliva and tears
Describe how to diagnose Sjogrens Syndrome?
Complex – no single test yet gives ‘the answer’
Balance of probabilities from multiple criteria
Different scoring systems in use:
- American-European Consensus Group (2002)
- ACR-EULAR joint criteria (2016)
Describe the diagnosis crietria for AECG of Sjogrens syndrome?
Dry eyes/mouth
- Subjective or objective
Autoantibody findings
Imaging findings
Radio nucleotide assessment
Histopathology findings
FOUR or more positive criteria for diagnosis
Describe the diagnosis crietria for ACR-EULAR of Sjogrens syndrome?
Histopathology findings (Weight 3)
focus score >1
Autoantibody findings (Weight 3)
anti-Ro
Dry eyes/mouth (Weight 1)
- objective salivary flow
- Schirmer test
Ultrasound/sialogram now accepted as well (2020)
Same exclusion criteria as AECG but also IgG4 disease
Describe the oral and eye symptoms necessary to aid diagnosis?
Oral
Daily feeling of a dry mouth for >3 months
Recurrent swelling of salivary glands as an adult
Frequently drink liquid to aid swallowing dry foods
Ocular
Persistent troublesome dry eyes for >3 months
Recurrent sensation of sand/gravel in the eyes
Tear substitutes used >3 times day
Name the 2 eye tests for Sjogrens Syndrome?
Abnormal Schirmer test
<5mm wetting in 5 minutes
Fluorescein Tear film assessment
Name the oral test for Sjoregns Syndrome?
Abnormal UNSTIMULATED whole salivary flow (UWS)
<1.5ml in 15 mins
Explain to autoimmunity involved with Sjogrens Syndrome?
What do positive autoantibodies here mean?
- NOT CAUSATIVE in the disease process
- ASSOCIATED with the clinical pattern
- Antibodies possible without disease – need clinical and lab findings
Anti-Ro and Anti-La antibodies
- Collection of proteins found in the cell
- Different ones found in different patients Ro52 (70%), Ro60 (40%) and La48 (50%)
Other Autoantibodies?
- Other Extractable Nuclear Antigens (ENA) not associated
- ANA and RF not associated with Sjögrens
Explain the typical findings in a positive labial gland biospy for Sjogrens Syndrome - AECG?
Collection of >50 lymphocytes around a duct = Lymphocytic Focus
Generalised lymphocytic infiltrate is ‘non-specific sialadenitis’
>1 Focus Score (FS) consistent with Sjogren’s Syndrome
Thought to be the MOST diagnostic feature on ACR-EULAR criteria
Describe the procedure in which to start to process of Sjogrens Syndrome, if suspicious?
First, look in the patient’s mouth
- Sjogren’s patients complaining of dryness will have a dry mouth
- Early Sjogren’s patients will NOT have a dry mouth, nor complain of one
Do the least harmful tests first
- UWS in 15 mins - <1.5ml
- Anti-Ro antibody
- Salivary USS
- Baseline MRI of major salivary glands – for comparison for future lymphoma screen
If still equivocal do labial gland biopsy
- Risk of area of skin numbness following procedure
- Informed consent needed
LGB and Anti-Ro may be the ONLY positive results in early Sjogren’s
Describe the management for a patient suffering with Sjogrens Syndrome?
If patient presenting with a dry mouth and salivary deficit
- Gland function is already very low
- Oral Health needs paramount – diet, OHI, 5000ppm toothpaste
- Symptomatic treatment of oral dryness
- Salivary stimulants - pilocarpine?
If patient presenting early – NO dry mouth yet – active gland disease
- Liaise with rheumatologist – multisystem disease
- Consider Immune modulating treatment – hydroxychloroquine, methotrexate
Name the 3 categories of complications for patient living with Sjogrens Syndrome?
Effects of Oral Dryness
- caries risk, denture retention, infections, functional issues –speech/swallow
Salivary enlargement - Sialosis
- can occur at any time – usually permanent
- Reduction surgery possible but not advised – other health issues
Lymphoma risk
- Salivary lymphoma may present with unilateral gland swelling at any stage
- Increased general lymphoma risk too
- Screening? Who should review – generally the GDP with patient awareness
Examination of the salivary gland locations?
Extra oral examination
- Major salivary glands
Intraoral examination
- Minor salivary glands
- Duct orifices
- Fluid expression
What is the function of saliva?
Acid buffering
Mucosal lubrication
- Speech
- Swallowing
Taste facilitation
Antibacterial
Name the 5 main causes of a dry mouth?
Salivary Gland disease
Drugs
Medical Conditions & Dehydration
Radiotherapy & cancer treatments
Anxiety & Somatisation Disorders
How does salivary gland changes with age between 17-90yrs old?
Acinar tissue loss
37% Submandibular
32% Parotid
45% Minor glands
Describe in/direct effect on salivation?
Indirect effect
- External to the gland
Direct Effect
- Problems within the gland itself
Name 6 drugs that cause indirect salivary problems?
Anti-muscarinic cholinergic drugs
- Tricyclic antidepressant
- Antipsychotics
- Antihistamine
- Atropine
- Diuretics
- Cytotoxics
Name the 3 largest influencing drugs on dry mouth?
Antimuscarinic
- Amitriptyline 26% reduction
Diuretics
- Bendrofluazide 10% reduction
Lithium
- 70% have a significant reduction
- Increased caries correlates with drug use
Name other medical conditons that can have an indirect effect on salivation? - acute and chronic?
Chronic Medical Problems inducing dehydration
- Diabetes – Mellitus & Insipidus
- Renal disease?
- Stroke
- Addison’s Disease
- Persisting Vomiting
Acute medical Problems
- Acute oral mucosal diseases
- Burns
- Vesiculobullous diseases
- Haemorrhage
Name 5 direct salivary gland problems?
Aplasia
- Ectodermal dysplasia
Sarcoidosis
HIV disease
Gland infiltration
- Amyloidosis
- Haemochromatosis
Cystic Fibrosis
What is the defintion of ectodermal dysplasia?
Hair, Nails, Teeth, Salivary & Sweat glands
- Hearing and vision may be affected
May be limited in effect
- Salivary aplasia alone
Hypohidrotic – x-linked
Describe the symptoms of Sarcoidosis?
Haemachromatosis?
HFE gene mutation - 1:10 pop carry
Describe radiotherapy effect on salivation?
Radiation effects
Graft versus host effects
Antineoplastic drugs
Radioiodine
Describe Challacombe Scale of Mucosal Dryness?
What blood tests and other tests can be used to investiagte salivary disease?
Blood tests
- FBC
- U&Es,
- Liver function tests
- C-reactive Protein
- Glucose
- Anti Ro Antibody
- Anti La Antibody
- Antinuclear Antibody
- Complement C3 and C4
Functional Assay– Salivary Flow
Tissue Assay – Labial Gland Biopsy
Imaging
- Plain radiographs – reduced dose – stones
- Sialography – contrast to show ducts
- MR Sialography – IV contrast
- Ultrasound
Describe how anxiety and somatisation disorders can cause dry mouth?
‘cephalic’ control of salivation
- Inhibition of salivation – anxiety directly causes ‘real’ oral dryness
‘cephalic’ control of perception
- Altered perception of reality – normal information coming from the mouth is ‘misunderstood’ by small changes at synapses as it is processed
- More often seen with anxiety disorders
Anxiety can also inhibit swallowing and can lead to a complaint of ‘too much saliva’!
Name 6 forms of somatoform disease that cause dry mouth?
Oral Dysaesthesia
TMD pain
Headache
neck/back pain
Dyspepsia
Irritable Bowel Syndrome (IBS)
Flow rate normal vs abnrmal?
Name 5 treatbale causes of dry mouth?
Dehydration
Medicines with anti-muscarinic side effects
Medicines causing dehydration
Poor Diabetes control – type 1 or type 2
Somatoform Disorder – diagnosis of exclusion
Management of these should return the patient’s oral comfort
Name th 3 treatment options for symptomatic dry mouth?
Sjögren’s Syndrome
Dry mouth from cancer treatment
Dry mouth from salivary gland disease
Treatment options for these cases
- INTENSIVE DENTAL PREVENTION
- Salivary substitutes
- Salivary stimulants
Name the 5 categroeis of dry mouth investigations?
Salivary Flow tests – less than 1.5ml unstimulated flow in 15mins
Blood tests
- Dehydration – U&Es, Glucose
- Autoimmune disease – ANA, Anti-Ro, Anti-La (ENA Screen), CRP
- Complement levels – c3 and c4
Imaging
- Salivary ultrasound – looking for ‘leopard spots’ or sialectasis
- Sialography – useful where obstruction/ductal disease is suspected
Dry eyes screen
- Refer to optician for assessment of tear film (preferred)
- Schirmer test – tear flow less than 5mm wetting of test paper in 15 mins
Tissue examination
- Labial gland biopsy – lower lip – looking for lymphocytic infiltrate and focal acinar disease
Describe the dental management of dry mouth?
Prevent oral disease
- Caries risk assessment
- Candida/staphylococci awareness and reduction – low sugar diet and OHI
Angular chelitis
Sore tongue
Maximal preventative strategy
- Diet!
- Fluoride
- Treatment Planning for a caries risk mouth
Name 6 forms of saliva substitiues and their form?
Sprays
- Glandosane
- Saliva Orthana
Lozenges
- Saliva Orthana
- SST
Salivary stimulants
- Pilocarpine (Salagen)
Oral Care Systems
- Oral Balance
Frequent sips of water
Name the causes of hypersalivation? - True and percieved?
TRUE (rare) – Actual increase in salivary flow
- Drug causes
- Dementia
- CJD
- Stroke
PERCEIVED (Common) – NO increase in saliva flow
Swallowing Failure
- Anxiety
- Stroke
- Motor Neurone Disease
- Multiple Sclerosis
Postural Drooling
- Being a baby
- Cerebral Palsy
Describe the dental management of excess salivation?
Treat the Cause
- Anxiety disorders
Drugs to reduce salivation
- Anti-muscarinic agents
- Botox to prevent gland stimulation
Biofeedback training
- Swallowing control
Surgery to salivary system
- Gland removal
- Duct repositioning
Name the 3 forms of causes for changes in gland size?
Viral Inflammation
- Mumps
- HIV
Secretion retention
- Mucocele
- Duct obstruction
Gland Hyperplasia
- Sialosis
- Sjögrens Syndrome
Name the 7 symptoms of mumps?
Headache
Joint pain
Nausea
Dry mouth
Mild abdominal pain
Feeling tired
loss of appetite
Pyrexia of 38C, or above
Paramyxovirus
Droplet spread
Incubation 2-3 weeks
1/3 have no symptoms
Symptomatic treatment only
What is the defintiion of HIV sailvary disease?
HIV can be a cause of salivary swelling
Cause of Unexplained salivary swelling
May have NO HIV symptoms when presenting
Generally does not improve with treatment
Lympho-proliferative enlargement of the glands
What is the definition of a mucocele?
Secretion retention
- In the duct
- Extravasated into the tissues
RECURRENT swelling – bursts in days
- ‘salty taste’
Common Sites
Junction Hard/Soft Palate
Lower lip
What is the definition of subacute obstruction?
Swelling associated with meals
- increases as salivary flow starts
- reduces when salivary flow stops
Usually SUBMANDIBULAR
occ. Parotid
Can be slowly progressive – over weeks
Eventually fixed & painful
Cause – duct obstruction
- Usually duct blockage in submandibular
- Usually duct stricture in parotid
Name the 3 main causes of subacute obstruction?
Sialolith (stones)
‘mucous’ plugging
Ductal damage from chronic infection (scarring)
(Salivary stones, Duct stricture, Duct dilation, chronic non-specific sialadenitis)
Name the 5 investigations for subacute obstruction?
Low dose plain radiography
lower true occlusal
SIALOGRAPHY – when infection free
Isotope scan if gland function uncertain
Ultrasound assessment of duct system
What is the definition of duct dilation?
Defect prevents normal emptying
Micro-organisms grow and lead to persisting and recurrent sialadenits
Gland function gradually lost and persisting infection leads to gland removal
May follow Recurrent Parotitis of Childhood at age 20-30
Describe the management of subacute obstruction?
Surgical sialolith removal if practical
Sialography for ‘no stone’ cases – washing effect
Consider gland removal if fixed swelling
Describe the outcome for subacute obstruction?
Reformation of stone/obstruction
Deformity of duct – stasis & infection
Gland damage – low salivary flow, ascending infection
What is the definition of silalosis?
Increase in Gland Tissue (Hyperplasia)
- Sialosis
- Sjögrens Syndrome
Major gland enlargement
No identified cause
- Alcohol abuse
- Cirrhosis
- Diabetes Mellitus
- Drugs
What investigations can be carried out to diagnose Sialosis?
Blood tests
Glucose
FBC, U&Es, LFTs, bilirubin
BBV screen – HIV, Hep B, Hep C
AutoAntibody Screen
- ANA, anti-Ro, anti-La
Other investigtions
MRI of major salivary glands
USS for Sjögren’s changes
Labial gland biopsy
Tear film
Sialography – occasionally
Photography
What investigations can be carried out to diagnose Sialosis?
Blood tests
Glucose
FBC, U&Es, LFTs, bilirubin
BBV screen – HIV, Hep B, Hep C
AutoAntibody Screen
- ANA, anti-Ro, anti-La
Other investigtions
MRI of major salivary glands
USS for Sjögren’s changes
Labial gland biopsy
Tear film
Sialography – occasionally
Photography
Name 2 types of dental manifestations of systemic disease?
Disruption to the tooth structure formation
Disruption to the tooth structure content
Name 3 forms of systemic diseases that exhibit dental mnifestations in children?
Congenital conditions/infections
- Syphilis,TORCH
- Ectodermal Dysplasia
- perinatal illness
Illness/metabolic disorder
- Severe childhood illness - Porphria
- Cancer treatments
Pigmentation from substances in the blood
- Bilirubin, tetracycline
Name 6 oral mucosal effects from systemic disease?
Giant Cell Granuloma
Orofacial Granulomatosis
Recurrent Aphthous Stomatitis
Dermatoses
Immune Deficiency/Disease - Raised ACTH Addison’s
Drug reactions
What is the definition of a ginat cell lesion, in relation to oral medicine?
Peripheral’ and ‘Central’ lesions
Check Parathyroid function – could be as a result of excess parathyroid stimulation of osteoclasts
- renal failure
- hypocalcaemia
- parathyroid tumour
What is the definition of hyperparathyroidism’s effect on the bones?
Causes thinking and finger-like projections of the bone
Name 4 systemic illness that cause immunodeficiency throughout life, which show oral manifestations?
Orofacial Granuolomatosis
Sjogrens
Autoimmune – Addisons
Infections – fungal/viral
Name 2 forms of skin immune disease that show oral manifestations?
Lichen planus, VB disease
What is the definition of immune disease orofacial granulomatosis?
Associated with Dietary Allergens?
- Benzoate, Sorbate, Cinnamon, Chocolate (E210-219)
Skin testing not reliable
Use dietary exclusion to determine trigger (if any)
enzoates found in tomato and tomato products
- All things with tomato sauces must be avoided
Clinical signs:
- lip swelling, erythema and crustiness
- gingivae erythematous and heavly inflammed
What is included for Crohn’s screening?
Parental awareness of importance of altered bowel habit or abdominal pain
Growth monitoring at each hospital visit
Faecal Calprotectin assay
- Unreliable in younger children
- Screening test for endoscopy
- Good predictor of Crohn’s disease activity
Describe the management of orofacial granulamtosis?
Management
- 3 month empirical dietary exclusion
- Benzoate/cinnamon – unless clear other dietary triggers
Topical treatment to angular chelitis/fissure
- Miconazole/hydrocortisone cream
Topical treatment to lip swelling or facial erythema
- Tacrolimus ointment 0.03%
- Intralesional steroids to lip
- Systemic immune modulation?
Name 4 forms of automimmune CT diseases, that show oral manifestations?
Systemic lupus erythematosis (SLE) - erytheamic gingiva and palate
Systemic sclerosis (Scleroderma)
Sjogrens syndrome
Mixed connective tissue disease (MCTD)
Name 3 forms of vasculitic CT diseases, that show oral manifestations?
Large vessel Disease
- Giant cell (temporal) arteritis
Medium Vessel Disease
- Polyarteritis nodosa
- Kawasaki disease
Small vessel Disease
- Wegener’s Granulomatosis
Name 4 forms of acquired immune deficiency?
Diabetes
Drug therapy
Cancer therapy
HIV
What is the definition of haematinic deficieinces - causes?
Poor intake – dietary analysis/reinforcement
Malabsorbtion
- GI diseases – Coeliac Disease, Crohn’s Disease
Blood loss
- Crohn’s Disease, Ulcerative Colitis, Peptic ulcer disease, Bowel Cancer, Liver Disease
Increased Demand
- Childhood growth spurts
What is the definition of the Parotid gland?
Largest of major glands
Positioned parotid bed anterior to ear overlying mandibular ramus
Lower pole extends into postauricular region
Intimately associated with facial nerve (VII)
Serous gland. Produces thin watery secretion via parotid duct (Stensen’s duct)
WHat is the definition of the submandibular gland?
Second largest
Situated in submandibular triangle – associated with lower border of mandible, digastric and mylohyoid muscles and marginal mandibular branch of VII
Mixed seromucous (80% serous)
Expresses secretions via submandibular duct into floor of mouth (Wharton’s duct)
What is the definition of the sublingual gland?
Smallest major gland
Located in submucosa of floor of mouth
Nearby structures: submandibular duct, lingual nerve and lingual artery
Predominantly mucous
Expels secretions via Bartholin’s duct in floor of mouth
Name the 2 categories and 5 types of cells?
Acini:
- serous cells
- mucous cells
- mixed
Ducts
- Luminal cells: cuboidal/columnar/squamous epithelium
- Abluminal cells: myoepithelium and basal cells
What is the definition of neoplasia?
A neoplasm is an abnormal mass of tissue, the growth of which exceeds and is uncoordinated with that of the normal tissues and persists in the same excessive manner after cessation of the stimuli which evoked the change’
Benign
Malignant
Describe the epidemiology of salivary gland neoplasms?
Rare - 3/100,000
Commoner in women
75% benign
90% Parotid
Commnest parotid and minor- plemorphic adenoma
55% of palatal tumours - minor
50% of minor neoplasms are maligant
All sublingual glands are malignant
Name the 5 aetiologies of salivary gland neoplasms?
Radiation: nuclear bomb survivors, therapeutic radiation, dental x-rays, ?mobile phones
Tobacco smoking: Warthin’s tumour
Viruses: EBV & lymphoepithelial carcinoma
Familial and genetic
Various industrial occupations
Describe the differences between Benign and Malignant salivary gland tumours?
Benign
- Encapsulated
- Slow growing
- ‘Rubbery’ consistency
- Mobile
- Overlying mucosa/skin appears normal
- Not invasive
Incapable of metastasis Local excision curative Malignant - Unencapsulated - Rapid growth - Dense, firm mass - Fixed - Overlying skin/mucosa ulcerated Invades surrounding tissue including nerves Capable of metastasis Requires more aggressive therapy (surgery +/- radiotherapy)
Name 3 investigations for susected salivary gland tumours?
Clinical history and examination
Imaging: Radiography/Sialography, Ultrasound, CT, MRI
Pathology: Fine Needle Aspiration (FNA), core biopsy, open incisional biopsy, excisional biopsy
IMAGING AND PATHOLOGY ARE NOT A SUBSTITUTE FOR ADEQUATE HISTORY AND EXAMINATION
Name 5 types of benign epithelial tumoirs of the salivary gland?
Pleomorphic adenoma
Warthin’s tumour
Basal cell adenoma
Canalicular adenoma
Oncocytoma
Name 5 types of malignant salivary gland tumours?
Mucoepidermoid carcinoma
Adenoid cystic carcinoma
Polymorphous adenocarcinoma
Carcinoma ex pleomorphic adenoma
Acinic cell carcinoma
What is the definition of a pleomorphic adenoma?
Pleomorphic adenoma is a tumour of variable capsulation characterized microscopically by architectural rather than cellular pleomorphism. Epithelial and modified myoepithelial elements intermingle most commonly with tissue of mucoid,myxoid or chondroid appearance.’
Explain the management for a pleomorphic adenoma?
Wide surgical excision recommended due to high rate of recurrence in inadequately excised tumours
Excision complicated by lobulated structure, presence of satellite nodules and loose myxoid consistency
Enucleation usually results in incomplete excision and recurrences
Parotid: optimum technique - superficial parotidectomy with preservation of facial nerve (extracapsular dissection technique developing)
Submandibular: resection of gland
Minor gland: wide local mucosal excision +/- bone
What is the definition of Warthin’s Tumour?
A tumour composed of glandular and
often cystic structures, sometimes with a
papillary cystic arrangement, lined by
characteristic bilayered epithelium, comprising
inner columnar eosinophilic or
oncocytic cells surrounded by smaller
basal cells. The stroma contains a variable
amount of lymphoid tissue with germinal
centres.
What is the aetiology of Warthin’s tumour?
Exclusively in the Parotid
Male predominance
Link with smoking
Explain the management of Warthin’s tumour?
Complete excision is curative (superficial parotidectomy)
What is the definition of a Oncocytoma?
Benign tumour of salivary gland origin
composed exclusively of large epithelial
cells with characteristic bright
eosinophilic granular cytoplasm (oncocytic
cells).
What is the aetiology of a Oncocytoma?
Most in parotid
Complete excision curative
What is the definition of a canalicular adenoma?
The tumour is composed of columnar
epithelial cells arranged in thin, anastomosing
cords often with a beaded pattern.
The stroma is characteristically paucicellular
and highly vascular.
What is the aetiology of a canalicular adenoma?
lip commonest
conservatice excision curative
What is the definition of a basal cell adenoma?
Basal cell adenoma (BCA) is a rare
benign neoplasm characterized by the
basaloid appearance of the tumour cells
and absence of the myxochondroid stromal
component present in pleomorphic
adenoma.
What is the aetiology of a basal cell adenoma?
Mostly Parotid gland
Complete excision curative
What is the definition of mucoepidermoid carcinoma?
Mucoepidermoid carcinoma is a malignant
glandular epithelial neoplasm characterized
by mucous, intermediate and
epidermoid cells, with columnar, clear
cell and oncocytoid features.
What is the aetiology of mucoepidermoid carcinoma?
most common saliary gland malignancy
Parotid most common, then palate, submand and other minors
Exlain the management of mucoepidermoid carcinoma?
Low grade: cystic, lots of mucous cells
High grade: solid, few mucous cells, atypia, mitoses++, perineural invasion, infiltrative growth and necrosis.
10 year overall survival rates:
low grade 90%
intermediate grade 70%
high grade 25%
What is the definition of an adenoid cystic carcinoma?
Adenoid cystic carcinoma is a basaloid
tumour consisting of epithelial and
myoepithelial cells in variable morphologic
configurations, including tubular,
cribriform and solid patterns. It has a
relentless clinical course and usually a
fatal outcome.
What is the aetiology of an adenoid cystic carcinoma?
High grade malignnacy
More in female
Major glands
Distant metastases
Explain the management of adenoid cystic carcinoma?
Surgery treatment of choice
Wide resection. Extensive surgery often required
Clear margins difficult to achieve (mostly impossible)
Radiotherapy with wide fields
Chemotherapy generally not effective
What is the definition of a polymorphous adenocarcinoma?
A malignant epithelial tumour characterized
by cytologic uniformity, morphologic
diversity, an infiltrative growth pattern,
and low metastatic potential.
What is the aetiology of a polymorphous adenocarcinoma?
2nd most common intraoral malignant salivary gland
Palate most commen
Malig in minor
Explain the management of polymorphous adenocarcinoma?
Surgical excision with clear margins usually curative
Role of radiotherapy not certain
What is the definition of Carcinoma ex pleomorphic adenoma?
Carcinoma ex pleomorphic adenoma is
defined as a pleomorphic adenoma from
which an epithelial malignancy is
derived.
What is the aetiology of carcinoma ex pleomorphic adenoma?
Usually arises from an untreated benign pleomorphic adenoma present for several years; most arise in the parotid gland
Presents as rapid swelling following an extremely long period of slow growth.
Slightly more common in women
Explain the management of carcinoma ex pleomorphic adenoma?
Extensive surgery with neck dissection is treatment of choice
Post operative radiotherapy
What is the definition of an acinic cell carcinoma?
Acinic cell carcinoma is a malignant
epithelial neoplasm of salivary glands in
which at least some of the neoplastic
cells demonstrate serous acinar cell differentiation,
which is characterized by
cytoplasmic zymogen secretory granules.
Salivary ductal cells are also a component
of this neoplasm
What is the aetiology of an acinic cell carcinoma?
Second most common salivary gland malignancy in children
Explain the management of an acinic cell carcinoma?
Complete excision required
Generally not aggressive but a proportion can metastasise to cervical lymph nodes and lung
Recurrence rate as high as 35%
