BAMS Oral Medicine Flashcards
Characteristics of healthy oral mucosa
Pink
Stippled
Moist
Lubricated
Normal anatomy that patients could report as disease
Taste buds
Tori
Parotid duct (lump in cheek)
Flabby ridge
Spotty bits
Geographic tongue
What are Fordyce spots?
Yellow or white spots
Sebaceous glands
60-75% of adults
Buccal mucosa and lips
No associated pathology
Linea Alba
Horizontal asymptomatic white lesion
Along occlusal plane
Histologically - hyperkeratosis, prominent or reduced granular layer, acanthosis
Geographic tongue
Variation of normal anatomy
Benign migratory glossitis/ Erythema migrans
3% of population
Asymptomatic
Sometimes sensitive to hot, spicy, toothpaste
Loss of filiform papillae
Comes and goes and changes appearance
Can affect other areas of mucosa
Reassure pt, rarely requires further intervention
Fissured tongue
Variation of normal anatomy
Can occur later in life
No treatment necessary
Food and debris can build up in fissures of tongue
Encourage good hygiene and lightly brushing tongue
Which two variations of normal anatomy are often concordant?
Geographic tongue
Fissured tongue
Black hairy tongue
Hyperplasia of filiform papillae
Build up of commensal bacteria and food debris
Pigment inducing fungi and bacteria
Largely asymptomatic
Reassure pt
Specific cause unknown
Factors associated with black hairy tongue
Smoking, antibiotics, chlorhexidine mouthwash, poor OH
Advice for black hairy tongue patients
Stop smoking
Stay hydrated
Lightly brush tongue
Gently exfoliate tongue - eg. peach stone
Eat fresh pineapple
Desquamative gingivitis
Not a specific diagnosis, a descriptive term meaning full thickness erythema of the gingiva
Not caused by plaque but exacerbated by it
Important to manage periodontal disease in these cases
Associated with lots of conditions
Consider biopsy
Bony exostosis
Usually benign overgrowth of calcified bone, can be associated with parafunction
30-40% of the population
Can be present on the palate, mandible or buccal alveolus
Can interfere with dentures
Typically painless
May be more prone to ulceration
Physiological pigmentation
Normal
More common in non-white ethnicities
Due to increased melanin pigmentation
Can make the diagnosis of mucosal disease more challenging
Consider - addison’s, smoker’s melanosis, drug related pigmentation
Mucosal disease appearance
White patches
Red patches
Brown patches
Ulcers
Blisters
Lumps and bumps
Salivary gland disease presentation
Hyposalivation
Hypersalivation
Swellings
Lumps and bumps
Possible causes of facial and unexplained oral pain
Joints
Glands
Trigeminal neuralgia
Neuropathic pain
Other non-dental pain
Ulcer
Localised defect where there is destruction of epithelium - a breach in the mucosa
Vesicle
Fluid filled lesion
Causes of ulcers
Traumatic
Metabolic/nutritional
Allergic/hypersensitivity
Infective
Inflammatory
Immunological
Drug induced
Neoplastic
Idiopathic
What can give a clue as to the cause of an ulcer?
Site
Onset
Duration
Number
Texture
Appearance
Size
Pain
Predisposing factors
Relieving factors
Traumatic ulcer
White keratotic border
Clear causative agent
Should be soft and surrounding mucosa normal
Movement disorders and sensory impairment can cause these, or chemical burns
Apthous ulcer
Most common ulcerative condition
Painful yellow centre with red border
20% of the population experience
Typically non keratinsed tissue such as labial or buccal mucosa, tongue
Recurrent apthous ulcers classification
Major - greater than 1cm and long time to heal
Minor - less than 1cm and heals 2-3 weeks
Herpetiform - multiple small ulcers that may coalesce
Apthous ulcer triggers
Stress, trauma, allergy, sensitivity, metabolic
To investigate anaemia
FBC, vit b12, folate, ferritin, coeliac screen
Behcet’s ulcers
apthous appearance but also involve skin, genitals and eyes to varying degrees
Common features of connective tissue disease
Joint pain and stiffness
Photosensitive rashes
Xeropthalmia/xerostomia
Fatigue
Infective causes of oral ulcers
Primary or recurrent herpes simplex virus
Varicella-zoster virus
Epstein barr virus
Echovirus
Coxsackie virus
Treponema pallidum
Mycobacterium tuberculosis
Chronic mucocutaneous candidiasis
HIV
Primary herpes simplex virus infection
Generally affects age 2-5
Associated with a fever, headache, malaise, dysphagia, cervial lymphadenopathy
Short lasting vesicle affecting lips, buccal, palatal and gingival mucosa then forming ulceration
Varicella zoster virus
Primary infection with virus (chicken pox) -> virus remains latent in sensory ganglion -> reactivation of the virus resulting in VCZ infection (shingles)
Reactivation often due to immunocompromisation or other acute infection
Liase with GMP
Provide analgesia and difflam if painful (benzydamine hydrochloride - NSAID)
Iatrogenic ulcer examples
Chemo
Radiotherapy
Graft versus host disease - presents identically to lichen planus
Drug induced - potassium channel blockers, NSAIDs, bisphosphonates, DMARDs
Features of an ulcer than increase suspicion of oral cancer
Exophytic
Rolled borders
Raised
Hard to touch
Unmoveable
Sensory disturbance
(Not always painful)
Management of oral ulceration
Refer urgently to OMFS if suspicious of malignancy
Reverse the reversible - smooth sharp cusps etc
Refer to GP for FBC/haematinics/coeliac screen - if apthous appearance
HSMW
Antiseptic mouthwash
LA - benzydamine spray or mouthwash
Steroid mouthwash (betamethasone)
Steroid inhaler (beclometasone)
Onward referral
Nociceptive pain example
Putting hand to hot pan - withdrawal reflex
Inflammatory pain example
Irreversible pulpitis
Pathological pain
Maladaptive - abnormal functioning of the nervous system
Example - oral dyaesthesia
Understudied
Often no cure
Four classic signs of inflammation
Dolor - pain
Calor - heat
Rubor - redness
Tumor - swelling
How to approach pain in oral med
History - many pain syndromes can be diagnosed from the history
Exclude dental pathology
- Exam
- Radiography
- Pulp vitality
Further investigations
- Blood investigations
- Cranial nerve exam
- MRI
Pain history
Site
Onset
Character
Radiation
Associated symptoms
Time
Exacerbating factors
Severity/sleep
Mucosal causes of pain
Ulcers
Lichen planus
Vesiculobullous disorders
Salivary gland pain
Neuropathic pain
Non diseased dentoalveolar structure
Burning/shooting/shock like/allodynia/hyperalgesia
Perhaps hypoaesthesia or dysaesthesia
Continuous with intermittent severe episodes
Clearly defined with no radiation
Burning mouth syndrome
Oral dyaesthesia
Pain/burning sensation
Altered sensation
Perception of dry or excess saliva
Common on the tongue
Normal mucosa
Doesn’t follow anatomical boundaries
Discomfort as opposed to pain
Trigeminal neuralgia
Electric shock/shooting/stabbing pain
Unilateral
Severe 10/10
Short lasting
Episodic
Rarely has concomitant pain
May or may not have triggers
Sometimes a cause - tumour, MS, neurovascular conflict
MRI is essential
Good improvement in symptoms with carbamazepine/oxcarbazepine
Contributing to colour of oral mucosa
Blood
Saliva
Thickness of epithelium
Ethnicity
Exogenous factors
Candida
Inflammation
Keratinisation
Possible explanation of white patch
Abnormal or increased keratin
Increase epithelial thickness
Candida
Keratotic tissue can not be wiped away
Diagnosis is achieved through histological and clinical features
Factors increasing risk of oral candidal infection
Immunosuppression - medication/medical condition
Poor denture hygiene
Antibiotics
Smoking
Steroid inhaler
Medical conditions such as diabetes
Management of oral candidiasis
Consider anti-fungal therapy - fluconazole, miconazole, nystatin
Local measures - rinse after inhaler, use a spacer, denture hygiene, smoking cessation
Fluconazole and miconazole have lots of drug interactions - sometimes GP will allow a statin holiday for a couple of weeks for antifungals
This is a chronic problem, unless immunocompromising or local factors are reversed it will likely return
Traumatic keratosis
Protective response
Increased keratin deposition at a site of trauma
Encourage smoking cessation
Get a photograph
Can you reverse traumatic element
If a high risk site or individual consider referral to secondary care
Oral lichen planus and lichenoid reactions
CD8+ T cell mediated destruction of basal keratinocytes
Chronic inflammatory condition - perhaps autoimmune but no autoimmune antigen detected
May be asymptomatic or present as burning or stinging sensation
Oral lichen planus - generalised and idiopathic
Oral lichenoid tissue reaction - localised and may be a response to medicines/allergens
Drugs that cause OLR
Antihypertensive
Antimalarials
NSAIDs
Allopurinol
Lithium
OLR/OLP symptomatic relief
HSMW
LA - bezydamine or lidocaine
Avoid trigger foods such as spice or fizzy
Steroids - betamethasone mw, beclometasone inhaler or hydrocortisone oromucosal tablets)
Change restorations?
Onward referral
Hairy Leukoplakia
Non removeable white patch most common on lateral borders of the tongue
Acanthotic and para-keratinised tissue, finger like projections of para keratic
Triggered by epstein barr virus
Typically in immunocompromise pts
Virus triggering hairy leukoplakia
Epstein barr virus
How is leukoplakia diagnosis made?
By exclusion of other possibilities in a clinical diagnosis
No obvious cause for white patch
Has malignant potential
Can be dysplastic
Requires biopsy for histological examination to reach this diagnosis
Atrophy
Tissue becomes thinner
Concern with red patches with no clear cause
High likelihood of being dysplastic or malignant
Granulomatosis with polyangiitis
Systemic vasculitis - can affect other systems (can affect other parts of the body such as eyes, lungs, nose, heart, skin, kidneys)
May have fever and weight loss
92% have ear, nose or throat manifestations
Potentially fatal
Managed with immunosuppressants
Erythroplakia
Velvety firey red patch
Diagnosis of exclusion
Cannot be attributed to another disease
Most will have dysplasia or malignancy
Urgent referral indicated
Granulomatosis disease
OFG, Oral Crohn;s
Non-necrotising granuloma formation
Clinically very similar
Consideration of GI investigation
Management principles - topical steroids, avoidance diets, intralesional steroid, biologics for Crohn’s disease (infliximab)
Erythroleukoplakia
Speckled white and red patches
High risk - refer urgently to secondary care
Aetiology the same as leukoplakia/erythroplakia
Clinical assessment of a white or red patch
Location
Colour
Homo/heterogeneity
Induration - hard or soft
Raised or flat
Texture
Wipeable
Symmetry
Unlicensed use of medicines
Often medicines used in OM are not licensed for the condition they are being used to treat, as they have been originally licensed for some other use, and getting them licensed for another use would be very expensive and time consuming as evidence of the use would have to be submitted to MHRA
Documents used to choose medication regime in primary care of oral medicine conditions
SDCEP and BNF
Types of medicines used in oral med
Anti microbials
Topical steroids
Occasionally systemic steroids
Dry mouth medications
Immunosuppressant/immunomodulatory
Antimicrobials categories
Antibiotics
Antifungals
Antiviral
Why are antiviral and antifungals used more than antibiotics in oral med?
They more commonly cause acute or chronic oral mucosal diseases
Classifications of medicines
General sale
Pharmacy
Prescription only
Controlled drugs
Medical devices
What classification are saliva substitutes and why?
Medical devices, they are used to treat or alleviate disease by replacement of a physiological process and does not achieve its primary intended action by pharmacological, immunological or metabolic means, fitting with the WHO definition of medical devices
Licensed medicine
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
Requires a lot of evidence such as clinical trial data and post license surveillance
Unlicensed medicines
Medicines that have not had evidence of efficacy submitted for the condition under tx. The company is not claiming the medicine is useful for the condition being treated, it will be licensed for another condition
Colchicine licensed and unlicensed use
Licensed for gout
Useful for oral ulceration
What is it important to give to a patient when prescribing a medication for off license use?
A tailored PIL, as well as telling them that this is unlicensed use
Acyclovir use in oral med
Anti viral used to treat primary herpetic gingivostomatitis, recurrent herpetic lesions, shingles (recurrent herpes zoster)
Antifungals in oral medicine
Miconazole, fluconazole, nystatin - used to treat acute pseudomembranous candidiasis, acute erythematous candidiasis
Beclomethasone in oral medicine
Metered dose inhaler licensed for asthma and COPD
Applied directly to the lesion as topical steroid
Used for treating aphthous ulcers and lichen planus
Two unlicensed uses of topical steroids in oral med
Beclomethasone inhaler and betamethasone mouthwash for aphthous ulcers and lichen planus
Examples of dry mouth treatments
Salivix pastilles
Saliva orthana
Biotene oral balance
Artificial saliva DPF
Glandosane
Potential drug regime for lichen planus and why?
Lichen planus is often a fungal infection on top of immunological change - tx starts with antifungal and is continued with topical steroid
Tricyclic antidepressants in oral med
Only prescribed by specialist in hospital setting, not GDP
Amitriptyline or nortriptyline
Mainly for oral facial pain
Work centrally in the CNS to reduce pain transmission
Anti epileptic drugs in oral med
Only in specialist hospital oral med, not GDP
Gabapentin or pregabalin
Mainly to treat oral facial pain, especially neuropathic pain
Examples of drugs used to treat inflammatory and immunological mucosal diseases when simple treatments have failed
Azathioprine or mycophenolate - immunosuppressants
Hydroxycholoroquine or colchicine - immune modulating
Considerations when prescribing medications in oral med
Clinical indication
Licensed or unlicensed for this use - always favour licensed
Dose and route of administration - may vary from pt to pt
Important warnings for the pt such as alcohol and metronidazole
Drug interactions and cautions such and antifungals with statins
Treatment duration and monitoring - with some immune modulating drugs it is necessary that pt has regular blood tests in clinic or with GP
Must include in prescription
Pts name, address, age
Patient identifier - DoB CHI
Number of days tx
Drug to be prescribed
Drug formulation (tablet, capsule, suspension) and dosage
Instructions on quantity to be dispensed
Instructions to be given to the patient
Signed by dentist
How long is a prescription valid for?
6 months from date issued
This is useful to know when prescribing for a pt that may be away from the clinic for a while, or for a pt who only need medication upon occurrence of the condition e.g. recurrent herpetic lesions
Why is it important to give written instructions when prescribing medication?
Pt may be stressed during appt and not remember
Language issues may prevent proper understanding, multilingual, large print options
Provide contact number for patient issues with the medicine
Legal protection if post treatment course questioned
Advice to patients when prescribing medication
Take drugs at correct time and finish the course
If unexpected reactions - STOP and contact prescriber
Known side effects should be discussed eg metronidazole and alcohol
Keep medicines safe especially from children
Non steroid topical treatment of oral mucosal lesions
Chlorhexidine mouthwash (dilute with 50% water if needed)
Benzydamine mouthwash or spray - useful topical anaesthetic
OTC remedies such as igloo, listerine, bonjela
Steroid based topical treatment of oral mucosal lesions
Hydrocortisone mucoadhesive pellet
Betamethasone mouthwash
Beclomethasone metered dose inhaler
Betamethasone use for oral mucosal lesions
Use Betnesol 0.5mg tablets
1mg/two tablets in 10mls/2 teaspoons water
2 mins rinsing
Twice daily
Refrain from eating or drinking for 30 mins after use
DO NOT SWALLOW
Do not rinse after use
Provide tailored PIL for unlicensed use
Items for betamethasone mouthwash PIL
This is an accepted and proven effective treatment for the condition
Licensed for other medical conditions (over 12 years of age, use with caution below this age)
Explain dose range and frequency of use
Explain hazards of exceeding standard dose
Safe to use as directed without standard steroid side effects risk
Add any known side effects - small risk of oral candida
Add special instructions
MUST spit out to avoid systemic steroid effects, don’t rinse after use
Beclomethasone use in oral medicine
Metered dose inhaler 50mcg/puff
Unlicensed use - supply pt with tailored PIL
Position device with exit vent directly over ulcer area
2 puffs 2-4 times daily
Don’t rinse after
Must be pressurised inhaler not a breath activated device
Items for PIL for beclomethasone MDI
This is an accepted and proven effective tx for the oral condition
Licensed for other medical conditions - asthma and COPD
Instruct to discard the manufacturers PIL
Explain dose range and frequency of use
Explain technique used for oral lesions - different than for lung conditions
Add any known side effects - small oral candida risk
Add special instructions - do not rinse after
Systemic steroid use in oral med
Specialists only
Prednisolone
Can be pulsed for intermittent troublesome ulcers - high dose/short duration 30mg 5 days, need to ensure not used too frequently, once per month
When does use of systemic steroids pose significant risks
If prolonged course or repeated short courses over many months (3 months continuous or gaps of 2 weeks or less between pulses of prednisolone)
Systemic steroid risks
Adrenal suppression - steroid dependency, taper dose don’t stop suddenly
Cushingoid features
Osteoporosis risk - bone prophylaxis - calcium supplement and bisphosphonate, DEXA bone density scan may be needed from time to time
Peptic ulcer risk - proton pump inhibitor prophylaxis
Mood/sleep alteration and mania/depression - very quick onset
Immune suppressants used in oral med
Hydroxychloroquine - mainly for lichen planus
Azathioprine
Mycophenolate
Immunotherapy in oral medicine
Adalimumab
Enterecept
Risk management with immunosuppressant and immune therapy use in oral med
Infection risks, cancer risks, adverse drug reactions
Only for use by a specialist
Always communicate proposed treatment to GP - may be medical issues about which the OM clinician is unaware
Patient preparation for systemic immunomodulatory treatments
Must ensure that immunosuppression will not harm the patient - pre existing medical condition not yet detected
BBV screen - hep b and c and HIV
FBC
Electrolytes
Liver function tests
Thiopurine methyltrasnferase - only for azathioprine use
Zoster antibody screen
EBV
Chest xray - signs of previous or active TB
Cervical smear up to date
Pregnancy test
Treatment planning for immunomodulatory treatment
Needs full consent from pt - alternative treatments tried or discussed
Patient information given and pt reviewed to discuss this
Short term risk - acute drug reaction
Long term risk - cancer risk increase, especially azathioprine and skin cancer
Effective contraception and 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
Referral of suspected malignancy
Refer ANYTHING the dentist thinks might be cancer or dysplasia to 2 week cancer referral pathway
Photograph the lesions
Orthokeratosis
Thickening of keratin layer with preserved keratinocyte maturation
Usually found in areas where trauma to mucosa is expected
Parakeratosis
Incomplete maturation of keratinocytes leading to abnormal retention of the nuclei in the cells of stratum corneum
Usually result from a change from the standard mucosal type for example lichen planus
Layers between lamina propria and keratin in the hard palate
Stratum corneum
Granulosum
Spinosum
Basal
Lamina propria
Which layers of the oral mucosal epithelium have cell division occurring within them?
Basal and suprabasal
Gross types of oral mucosa
Lining
Masticatory
Gustatory
What is present in the lamina propria that is not present in the oral epithelium?
Blood vessels
What does it suggest histologically, when cells lose purple staining?
Losing organelles
Life of a cell from the basal membrane of the epithelium
Progenitor cells are present in the basal membrane, offshoots of these cells mature as they spread up the epithelium, eventually becoming the cells of the stratum granulosum and then the flattened keratin cells of the surface
What does mitosis in cells of outer layers of the epithelium suggest?
Dysplasia
Why are 2d histological sections limiting when looking for mitosis in the outer layers of the epithelium, as an indicator of dysplasia?
IT is a 2d section of a 3d structure, sometimes if you see mitosis happening far up the epithelium its actually another bit of basal layer that just happens to be a bit further up
Serial sections may be required
Keratosis
Reactive change of the oral mucosa
Trauma to the surface at a low level causes the surface to react by increasing the thickness of the epithelium and surface protection
Acanthosis
Hyperplasia of stratum spinosum/thickening of the epithelium, usually as a reactive change to trauma or immunological damage
Often elongated rete ridges, due to hyperplasia of basal cells
Example condition which can cause acanthosis
Lichen planus
Rete ridges
Epithelium projections which penetrate into the dermis or lamina propria
Increase contact area between epithelium and lamina propria, help spread out masticatory stress, provide protective niches where keratinocyte stem cells reside
Atrophy of oral mucosa
Reduction in viable layers
Erosion of oral mucosa
Partial thickness loss through disease
Ulceration of the oral mucosa
Complete loss of epithelium in a patch, often has a fibrin surface
Oedema
Fluid build up
Intracellular or extracellular (spongiosis)
Blister in the oral mucosa
Vesicle or bulla
Collection of fluid either within or just below the epithelium
Normal changes to oral mucosa with age
Progressive mucosal atrophy - older people may have slightly thinner mucosa
Loss of tongue papilla is NOT age related, this is due to epithelial disease and should be investigated
Likely cause of smooth appearance of tongue
Atrophy and loss of papillae due to Iron or b group vitamin deficiencies
Consequences of tongue atrophy
Predisposes to infection and makes it easier for candida to get in
Benign mucosal condition affecting 1-2% of the population, less in children, desquamation, varied in pattern and timing
Geographic tongue
Hyperplasia of papillae, bacterial pigment
Black hairy tongue
What type of epithelium does the mucosa have?
Stratified squamous epithelium
Layer underneath epithelium in oral mucosa
Lamina propria
Gross types of oral mucosa
Lining
Masticatory
Gustatory
Haematinics
Iron
B12
Folate
Areas of keratinised epithelium
Gingiva
Hard palate
Dorsal surface of the tongue
Non keratinised epithelium
Soft palate
Inner lips
Inner cheeks
Floor of the mouth
Ventral surface of the tongue
Main purpose of keratin on mucosa
Protection
Histological difference between parakeratosis and orthokeratosis
Orthokeratosis does not show dark dots
Parakeratosis shows dark dots
Dark dots are flattened cell nuclei
Layers of keratinised epithelium
Stratum corneum
Granulosum
Spinosum
Basale
In keratinised epithelium, where does cell division take place?
Basal and suprabasal cells
Keratosis
Deposition of keratin on epithelium as a reaction to trauma - one of the most common trauma responses in the oral mucosa
Why to some lesions appear white?
Increased keratin obscuring the view of the blood vessels within the lamina propria
What occurs throughout the layers of the epithelium during keratosis reaction to trauma?
Keratosis - deposition of keratin layer
Acanthosis - hyperplasia of stratum spinosum
Elongated rete ridges - hyperplasia of basal cells, spreading into lamina propria
Acanthosis
Hyperplasia of stratum spinosum, increased thickness of this layer
What causes elongated rete ridges?
Hyperplasia of basal cells spreading into lamina propria, can be trauma response
When does parakeratosis occur?
With inflammatory or immune causes
When does orthokeratosis occur?
As a response to trauma in the mouth
Why does orthokeratosis have an appearance without dark dots histologically?
The cells placed by orthokeratosis are without nuclei, as they have preserved cell maturation
Why do parakeratosis cells have dark coloured dots histologically?
They have retained nuclei as a sign of delayed maturation of keratinocytes
Atrophy
Reduction in viable layers - red lesion
Trauma response
Erosion
Partial thickness loss - loss of upper layers, can appear red
Ulceration
Full thickness loss of epithelium entirely in the area
Yellow fibrin on the surface
Exposed lamina propria
Oedema
Fluid accumulation
Can be intracellular or intercellular
Vesicle
Small blister
Bulla
Large blister
Why can some areas of atrophy have yellow appearance?
Adipose tissue showing through e.g. in the cheeks
Dysplasia
Disordered maturation (growth) in a tissue
Cellular atypia
Changes within cells
What is the significance of grades of severity of dysplasia?
More sever grade means increased likelihood of becoming malignant
Progressive atrophy
Progressive thinning of epithelium and loss of layers happens all over the body with age, can be visible in the mouth
What is there a predisposition to with atrophy?
Infection
Common causes of atrophy
Age
Nutritional deficiencies - iron, b12, folate
How the oral mucosa responds to trauma depends on…
Irritation
Time
Person
Epithelial reactions to trauma
Keratosis
Atrophy
Erosion
Ulceration
Oedema
Blister
Fibrous tissue formation
Epulides
Soft tissue swellings/fibrous overgrowth on the gingivae ONLY
Reaction to chronic inflammation or chronic trauma
Can reoocur after removal if stimulus persists
What does it mean if the word peripheral is used to describe a soft tissue swelling?
It originates from the gingivae and not from the jaw bone
Management of pt with good OH who has sudden unexplained mobility of teeth
Must be investigated as there’s a chance it is a malignancy in the jaw bone
Most common cause of fibrous epulis
Subgingival calculus
Fibrous overgrowths
Localised gingival hyperplasia
Cell types and structures in fibrous overgrowths
Macrophages
Fibrin
Blood vessels
Granulation tissue
Plasma cells
Bone formation can occur
Keratinised
Hyperplastic epithelium
What happens if fibrous overgrowth is traumatised?
Areas of erosion or ulceration can occur
Vascular epulis
On the gingivae only - pyogenic granuloma if elsewhere on the body
Lesions containing a lot of blood vessels
Can be response to trauma
Features present in vascular epulis or pyogenic granuloma
Lots of blood vessels
Granulation tissue
fibroblasts
Ulcerated surface
Neutrophils
Pregnancy epulis
Pyogenic granuloma on the gingivae during pregnancy, hormonal cause
Management of pregnancy epulis
If removing a pregnancy epulis, wait til after the birth as it will become smaller and less vascularised
Where do giant cell lesions tend to occur?
More anterior
Lingual/palatal side
Cells present in giant cell lesions
Multinucleated giant cells
Haemosiderin - form of storage iron derived from erythrocyte breakdown
Fibroblasts
RBCs
Causes of giant cells
Unphagocytic material in lesion, so giant cells form from fused macrophages, which are much more efficient at removal
Local chronic irritation
Infective agents
Hormonal stimulation of cells
Autoimmune - sarcoidosis
Relationship between giant cell lesions in the mouth and in bone
They can be an extension of the same pathology occurring in the jaw bone, it may be after it has already eroded the alveolar bone to emerge at gingiva
Reactive hyperplastic lesions
Traumatic fibroma/fibroepithelial polyp
Collagen fibres and keratinised thick epithelium
Find out the cause
Fibrous overgrowths associated with dentures
Denture induced hyperplasia
Leaf fibroma
Papillary hyperplasia of palate - candida infection or pseudo-epitheliomatous hyperplasia
Management of denture induced hyperplasia
Improve the fit of the denture, fibrous ridges should regress
Papillary hyperplasia of the palate is associated with
Poor OH or denture hygiene
Poor denture fit
Candidal infection may be present
Drugs associated with fibrous overgrowth
Antihypertensive - calcium channel blockers
Antiepileptic - phenytoin
Immunosuppressants - cyclosporin
Treatment of drug induced fibrous overgrowths
Repeated gingivectomy may be necessary
Improve OH
What is the difference between a generalised fibrous enlargement and an inflammatory cause clinically?
Generalised - firm on palpation
Inflammatory would be soft
Pregnancy gingivitis
Hormonal, due to increased progesterone
Can occur with oral contraceptive pill
Not in HRT
Responds to oral hygiene measures - it is an exaggerated plaque response
Microscopic types of vascular lesions
Capillary - small blood vessels
Cavernous - larger, blood filled spaces
Hamartoma
Normal tissue and structure but number greatly increased or location is abnormal. Can affect any area of body
e.g. - odontome
Path of large haemangiomas
Run along the course of a particular nerve, and are unilateral
Intra oral haemangioma appearance
Blue lesion
What is pain?
An unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage
What is the McGill questionnaire?
A questionnaire designed to help understand the levels of pain a patient is experiencing
What 4 ways can pain be felt?
Nociception
Peripheral nerve transmission
Spinal modulation
Central appreciation
What is nociception?
Processing of noxious stimuli such as tissue injury or temperature extremes, causing pain to be experienced
Nerve associated with structures derived from the first pharyngeal arch
Trigeminal
Chronic regional pain CRPS
Delocalised pain
Spreads around anatomical boundaries
Bilateral
Gripping, tight, burning
Feeling of swelling and heat, colour change in overlying skin, autonomic changes
Significantly disabling
Nociceptive pain
Painful stimulus causes activity in neural pathways
Neuropathic pain
Initiated or caused by primary lesion or dysfunction in the nervous system
Nociceptive pain examples
Post op pain
Mechanical low back pain
Arthritis
Neuropathic pain examples
Trigeminal neuralgia
Central post-stroke pain
Nerve damage due to issues with vascular supply to peripheral nerves in diabetes
Postherpetic neuralgia
Herpes zoster infection causes damage to the nervous system, giving pain symptoms
Neuropathic pain description
Constant burning/aching
Fixed location
Often fixed intensity
2 most common causes of neuropathic pain
Postherpetic neuralgia
Diabetic peripheral neuropathy
Traumatic causes of neuropathic pain
External injury
Nerve compression
Inflammation
Disease processes that can cause neuropathic pain
Infection/inflammation
Neurotoxicity
Tumour infiltration
Metabolic abnormality
Genetic causes for neuropathic pain
Inherited neurodegeneration
Metabolic/endocrine abnormalities
Therapeutic intervention causes for neuropathic pain
Surgery
Radiation
Chemotherapy
Topical medication for neuropathic pain
Capsaicin
EMLA
Benzdamine
Ketamine
Systemic medication for neuropathic pain
Pregabalin
Gabapentin
Tricyclic
Physical methods of neuropathic pain management
TENS
Acupuncture
Psychological management techniques of neuropathic pain
Distraction
Correct abnormal illness behaviour
Improve self esteem/positive outlook
Atypical odontalgia
Dental pain without dental pathology
Describes symptoms like acute pulpitis
Pattern of pain atypical odontalgia
Equal sex distribution
Pain free or mild between episodes
Intense unbearable pain 2-3 weeks
Settles spontaneously
Oral medicine care of atypical odontalgia chronic stategy
Reduce chronic pain experience
Reduce frequency of acute episodes
Oral medicine management of atypical odontalgia acute strategy
Have a plan to control pain
Opioid analgesics as required
High intensity/short duration
Persistent idiopathic facial pain
Pain which poorly fits into standard chronic pain syndromes
Often high disability level
What does high disability level of pain suggest
High level of autonomic component
Oral dysaesthesia
Abnormal sensory perception in absence of abnormal stimulus
Predisposing factors for oral dysaesthesia
Deficiency
- Haematinics
- Zinc
- Vit B1 and B6
Fungal and viral infections
Anxiety and stress
Gender - more women than men
Haematinics
Substance essential to the proper formation of the components of blood
Folic acid, vit b12, iron
Burning mouth syndrome
Oral dysaesthesia most likely to be associated with haematinic deficiency
SITE is important
Parafunction - more likely to get burning tongue tip and edges
Dysaesthesia - multiple other sites
Dysgeusia
Bad taste/bad smell dysaesthesia
Pt reports halitosis but nothing is found by clinician
REMEMBER smell could have ENT cause such as chronic sinusitis, perio/dental infection, GORD, it can be helpful to eliminate these
Touch dysaesthesia
Pins and needles tingling
Normal sensation to objective testing - pin/needle elicits pain
Cranial nerve test essential
Must exclude local causes of infection or tumour
MRI essential to ensure there is no demyelination or tumour
Dry mouth dysaesthesia
Most common
C/o debilitating dry mouth but can eat ok
Worse when waking at night
Usually the most obviously associated with anxiety
No positive findings to Sjogren’s tests
Management of dysaesthesia
Explain the condition to the patient - pins and needles, looks normal, feels weird
Assess degree of anxiety - clinical psychology or anxiolytic medication
Treatment empower the patient - control is important
Anxiolytic medication (nortriptyline, mirtazepine, vortioxetine) or neuropathic medication (gabapentin/pregabalin, clonazepan (topical?)) can be used
Expected cause of TMJ pain, crepitus
Joint degeneration
Expected cause of TMJ locking
Internal joint derangement
Physical signs TMD
Clicking joint
Locking
Limitation of opening
Tenderness of MoM
Tenderness of cervico-cranial muscles
Deviation on opening
Management of TMD
Information on how to self help
Physical therapy
CBT
Soft diet and analgesia
Bite splint
Biochemical manipulation - tricyclic (not SSRIs)
Other anxiolytic medication
Physiotherapy
Acupuncture
Clinical psychology
Neuralgia
An intense stabbing pain
The pain is usually brief but may be sever
Extends along the course of the cranial nerve affects
Can be due to irritation or damage of the nerve
Most common form is trigeminal
Nerves that can be affected by neuralgia
Trigeminal
Glossopharyngeal and vagus
Nervus intermedia
Occipital
Trigeminal neuralgia epidemiology
4.3 in 100000
More female
predominantly over 60s
Trigeminal neuralgia causes
Idiopathic
Classical (most common) - vascular compression of the trigeminal nerve
Secondary - multiple sclerosis, space occupying lesions (common) others, less common - skull base bone deformity, connective tissue disease, arteriovenous malformation
Trigeminal Neuralgia presentation
Stabbing pain
Tends to be unilateral
Tends towards maxillary or mandibular divisions of the trigeminal nerve over the ophthalmic division
5-10 seconds in duration
Each attack is a group of stabs
Can be purely paroxysmal or with concomitant continuous pain
Can go into remission and relapse
Triggers of trigeminal neuralgia
Cutaneous triggers
Wind, cold
Touch
Chewing
Trigeminal neuralgia typical patient
Usually older
Mask like face
Appearance of excruciating pain
No obvious precipitating pathology
Trigeminal neuralgia red flags
Younger patient <40
Sensory deficit in facial region - hearing loss, acoustic neuroma
Other cranial nerve lesions
ALWAYS test cranial nerves (identify sensory deficit)
MRI
Trigeminal neuralgia first line drug therapy
Carbamazepine
Oxycarbamazepine
If not tolerated, lamotrigine
Trigeminal neuralgia second line drug therapy
Gabapentin
Pregabalin
Phenytoin
Baclofen
Surgery indications for trigeminal neuralgia
When approaching maximum tolerable medical management even if pain controlled
Younger patients with significant drug use
Painful trigeminal neuropathy
Pain localised to the distributions of the trigeminal nerve
Commonly described as squeezing, burning or likened to pins and needles
More continuous pain
Trigeminal Autonomic Cephalalagias
Unilateral head pain
Predominantly V1 ophthalmic branch
Excruciating - suicide headache
Attack frequency and and duration differs
Usually other symptoms like eye odeoma, nasal congestion on ipsilateral side of face
Cluster headache
Mostly orbital and temporal region
Strictly unilateral
Rapid onsent
Duration 15m to 3hours
Rapid cessation
Patients are restless and agitated
Cluster over 1-3months with period of remission at least 1 month
Can be continuous background pain or symptomless
When is non steroid topical therapy used?
For inconvenient lesions with discomfort
When is steroidal topical therapy used?
For disabling immunologically driven lesions
Non steroid topical treatments for oral mucosa lesions
Chlorhexidene mouthwash
Benzdamine mouthwash or spray
OTC remedies like Igloo, bonjela
Steroid based topical treatments for oral mucosal lesions
Hydrocortisone mucoadhesive pellet
Betamethasone mouthwash
Beclomethasone MDI
Steroid side effects
Diabetes
Osteoporosis
Adrenal suppression
Dose of beclomethasone MDI for oral mucosal lesions
2 puffs over the ulcer area 2-4 times daily
Do not rinse
Systemic steroid used in oral medicine
Prednisolone
Systemic disease modulator used in oral medicine
Colchicine
Immune suppressants used in oral medicine
Hydroxychloroquine
Azathioprine
Mycophenolate
Immunotherapy drugs used in oral medicine
Adalimumab
Enterecept
Risks of systemic immunomodulatory treatments
Infection risks
Cancer risks
Adverse drug reactions
Patient preparation for systemic immunomodulatory treatments
BBV screen
FBC
Electrolytes
Liver function tests
Thiopurine methyltransferase for azathioprine use
Zoster antibody screen
EBV
Chest Xray
Cervical smear up to date
Pregnancy test
What is the disease which increased risk is specifically associated with azathioprine use?
Skin cancer
Extra-oral swelling differential diagnosis
Trauma
Dental infection
Sialosis
Ranula
Suppurative sialadenitis
Viral sialadenitis
Crohn’s
Orofacial granulomatosis
Salivary gland tumour
Squamous cell carcinoma
Paget’s disease
Fibrous dysplasia
Acromegaly
What appearance do these differential diagnosis have in common?
* Fibroepithelial polyp
* Drug induced hyperplasia
* Crohn’s disease
* Orofacial granulomatosis
* Warts and condylomata
* Focal epithelial hyperplasia
* Squamous cell carcinoma
* Salivary gland tumour
Intra oral pink swelling
Pyogenic granuloma
Giant cell granuloma
Denture induced hyperplasia
Scurvy
Squamous cell carcinoma
are differential diagnosis for what appearance?
intra oral red swelling
What appearance do these differential diagnosis have in common?
Squamous papilloma
Squamous cell carcinoma
Intra oral white swelling
Intra oral blue swelling differential diagnosis
Mucocele
Ranula
Intra oral yellow swelling differential diagnosis
Bony exostoses
Sialolith
Appearance for these differential diagnosis
* Amalgam tattoo
* Haemangioma
* Melanocytic nevus
* Melanotic macule
* Malignant melanoma
Kaposi’s sarcoma
Pigmented lesions, single or localised area
Appearance for these differential diagnosis
* Black hairy tongue
* Drug-induced pigmentation
* Smoker-associated pigmentation
* Physiologic pigmentation
* Hereditary haemorrhagic telangiectasia
* Sturge-weber syndrome
* Addison’s disease
* Betel nut/paan chewing
* Peutz-Jegher’s syndrome
* Thrombocytopenia
Multiple or widespread pigmented lesions
Description of lesions with these differential diagnosis
* Chemical burn (such as aspirin)
* Lichen planus
* Lichenoid reaction
Lupus erythematous
Painful white patches
What type of lesion would have these differential diagnosis?
* White sponge nevus * Dyskeratosis congenita * Frictional keratosis * Nicotinic stomatitis * Leukoplakia * Pseudomembranous candidiasis * Chronic hyperplastic candidiasis * Pyostomatitis vegetans * Skin graft * Hairy leukoplakia * Squamous cell carcinoma * Submucous fibrosis
Painless white patches
What would the appearance of these differential diagnoses be?
* Erosive lichen planus * Post radiotherapy mucositis * Contact hypersensitivity reaction
Painful, may ulcerate, red patches
What appearance would these differential diagnoses have?
* Iron deficiency anaemia * Pernicious anaemia * Folate deficiency * Angular cheilitis * Acute erythematous candidiasis * Geographic tongue * Medan rhomboid glossitis
Painful, no ulceration, red patch
What appearance would these differential diagnoses have?
* Infectious mononucleosis * Squamous cell carcinoma
Painless, may ulcerate, red patches
What appearance would these differential diagnoses have?
Erythroplakia
Chronic erythematous candidiasis
Painless, no ulceration, red patch
Common appearance of these differential diagnoses
* Traumatic ulceration * Minor or major recurrent aphthous stomatitis * Cyclic neutropenia * Behcet's disease * Tuberculosis * Syphilis * Squamous cell carcinoma * Necrotising sialometaplasia
Single or small number of discrete ulcers
Differential diagnosis
* Acute necrotising ulcerative gingivitis * Herpetiform recurrent aphthous stomatitis * Behcet's disease
Multiple discrete ulcers
Differential diagnosis
* Erosive lichen planus
* Lichenoid reaction
* Graft versus host disease
* Radiotherapy induced mucositis
Osteoradionecrosis
Multiple diffuse ulceration
Differential diagnosis
* Chicken pox * Hand foot and mouth disease * Herpangina * Primary herpetic gingivostomatitis * Recurrent herpes simplex infection * Mucocele
Blistering in children/young adults
Differential diagnosis
* Shingles * Pemphigoid * Pemphigus * Erythema multiforme * Linear IgA disease * Dermatitis herpetiformis * Angina bullosa haemorrhagica
Blistering in adults/elderly
Clinical findings dry mouth
Dry appearance, stringy foamy saliva, mirror sticks to tongue or buccal mucosa
Patient history for dry mouth
Medications
Dehydration
Drinking and smoking
Mouth breathing
Anxiety
Cancer treatment
Health conditions
Home management advice for dry mouth
Drink water
Suck ice cubes or sugar free sweets
Chewing gum
Humidifiers
Reduce caffeine and alcohol and foods that cause irritation
Use SLS free toothpaste
Irritant foods
Spicy or citric
Management of dry mouth in practice
Regular check ups to assess dryness and check for caries
Fluoride application
Prescribe 2800 or 5000 ppmF- toothpaste, mouthwash, gels, sprays, lozenges, sialalogues
Saliva orthana recommended after radiotherapy or in Sjogren’s syndrome
Be wary of Glandosane as it is acidic and erosive in the dentate
Review on a regular bases
Pt should be advised of the increased risk of decay, gum disease, poorly fitting dentures and fungal infections and so encouraged to come for regular checks
Drugs with dry mouth side effects
Beta blockers
Anti convulsants
Analgesics
Anti-emetics
Parkinson’s drugs
Diuretics
Anti-depressants
Antihistamines
Anti-psychotics
Anti-manic drugs
Beta blockers example
Propanolol
Atenolol
Anti convulsant drug example
Carbamazepine
Gabapentin
Phenytoin
Phenobarbital
Prescription analgesics examples
Morphine
Oxycodone
Anti-emetics examples
Pepto bismol
Sodium citrate
Dexemethasone
What is Levodopa?
dopamine replacement agent for the treatment of Parkinson disease
What is furesimide?
A diuretic used to treat high blood pressure (hypertension), heart failure and a build up of fluid in the body (oedema)
Anti histamines examples
Loratadine
Fexofenadine
Chlorpheniramine
Anti depressants examples
Amitriptyline
Citalopram
Fluoxetine
Anti psychotic drug examples
Clozapine
Phenothiazine
Anti manic drug example
Lithium
Medications which side effects of oral ulcers
NSAIDS
Beta blockers
Methotrexate
Penicillin
Nicorandil
Allopurinol
Sulphonamides
Sulfasalazine
Gold
Anti convulsants
Systemic conditions with oral ulcerations as a potential manifestation
Herpetic gingivostomatitis (HSV-1)
Lichen planus
Vesiculo-bullous conditions - mucous membrane pemphigus and pemphigoid
Hand, foot and mouth disease
Haematological malignancy (leukaemia)
Squamous cell carcinoma
Erythema multiforme
Haematinic deficiency
Inflammatory bowel disease - coeliac, crohn’s
What virus causes hand, foot and mouth disease?
Coxsackie virus
Home management of oral ulceration
Soft diet
Avoid irritant foods
Drink cool drinks through a straw and avoid hot drinks
Use soft toothbrush with SLS free toothpastes
Warm salty MW
Ice cubes over sores
OTC numbing gels
Antiseptic MW - chlorhexidine or peroxide based
Benzydamine MW or spray
Management in practice of oral ulceration
Adjust ill fitting dentures and sharp cusps/restorations
Prescribe mouthwashes, gels or sprays if needed
Refer to GMP if recurrent or cannot be managed by GDP - advise pt to keep ulcer diary
Refer for testing e.g. haematinics, gut function, gluten sensitivity, immune testing
Review at 3w and refer if necessary
What should you advise pt to write in an ulcer diary?
Duration
Site
Trigger
Anything else noticed
How are oral candidiasis conditions diagnosed?
Based on history and clinical findings
Look at appearance, note colour, site, distribution, symptoms, duration
Take a MH including conditions, medications, social history and denture hygiene routine and denture fit
Acute pseudomembranous candidiasis appearance
Oral thrush
White patches (milk curds) that can be wiped off to reveal bleeding bases, cheeks, palate, oropharynx, usually painless
Treatment of acute pseudomembranous candidiasis
Identify and address underlying cause - diabetes, HIV, antibiotic use, smoker
Improve OH - chlorhexidine, antifungals (miconazole 2.5ml 4x daily until at least 7 days after healed, or nystatin rinse 4x daily 7 days until 48h after healed, fluconazole most effective, dose depending on age)
Chronic hyperplastic candidiasis
Candidal leukoplakia (chance of malignancy)
Associated with heavy smokers, iron, b12 or folate deficiency
Appearance - white patch on commissures, buccal mucosa, or dorsum of tongue
Treatment - biopsy, check vitamin levels, stop smoking advice, 2-4 weeks oral fluconazole
Acute erythematous/atrophic candidiasis
Appearance - red shiny atrophic mucosa
Cause - chronic use of antibiotics, steroid inhalers, immunosuppression, xerostomia
Treatment - spacer device/rinse after inhaler
Identify and address underlying cause - diabetes, HIV, antibiotic use, smoker
Improve OH - chlorhexidine, antifungals (miconazole 2.5ml 4x daily until at least 7 days after healed, or nystatin rinse 4x daily 7 days until 48h after healed, fluconazole most effective, dose depending on age)
Chronic erythematous candidiasis
Denture stomatitis
Appearance - diffuse redness in denture bearing area, asymptomatic
Treatment - denture hygiene advice, soak denture in sodium hypchlorite/chlorhexidine, miconazole gel 5-10ml to affected area 4x daily until 48h healed
Refer to GMP if suspect systemic cause (vitamin levels, medications, endocrine)
Angular chelitis cause
Trauma, immunosuppression, malabsorption, iron/b12 deficiency, broad spectrum antibiotics, candida infections, incorrect OVD dentures
Treatment of angular chelitis
Correct the cause
Topical miconazole, continue 10 days after healed
Methotrexate
Immunosuppressant prescribed for inflammatory conditions including rheumatoid arthritis
Side effect of oral ulceration
Nicorandil
Vasodilator used to treat angina
Side effect of oral ulceration
Prescription lithium
Mood stabilising/anti manic drug
Side effect of dry mouth
Levodopa
Parkinson’s drug
Dopamine replacement agent used to control bradykinetic symptoms
Side effect of dry mouth
Allopurinol
Drug used to prevent or lower high uric acid levels in the blood which can be caused by cancer treatment or kidney stones, as this could lead to gout
Side effect of oral ulceration
When are medications containing gold most likely to be used?
Rheumatoid arthritis pt
Side effect of oral ulceration
Sulphonamides
Group of drugs used to treat bacterial infections
Side effect of oral ulceration
Sulfasalazine
Drug used to treat inflammatory bowel diseases (UC, Crohn’s) and rheumatoid arthritis
Side effect of oral ulceration
Name the three main, but not unique clinical features of Sjogren’s
Dry eyes and mouth
Fatigue
Joint pain
2 most common antigens found in Sjogren’s
Anti Ro and Anti La
or SS-A and SS-B
Name the two clinical tests to measure the quantity of saliva and tears that are essential items included in the classification criteria of SS ACR/EULAR 2016
Unstimulated salivary flow test
Schirmer’s test
Oral signs and symptoms is Sjogrens
Salivary hypofunction
Caries
Oral fungal infection
Dysphagia
Dysgeusia
Salivary gland enlargement
Most common medication used for stimulating salivary glands in Sjogrens
Pilocarpine
Most common malignancy associated with Sjogrens
Non-hodgkins lymphoma
Histopathological features of a minor salivary gland biospy in sjogrens
Lymphocytic focus particularly periductal area
Atrophy of acini
Fibrosis
Ductal dilation
Ductal epithelial hyperplasia
What is neuralgia?
Intense stabbing pain
Pain is usually brief but may be severe
Pain extends along the course of the affected nerve
Usually caused by irritation of or damage to a nerve
Causes of trigeminal neuralgia
Idiopathic
Classical - vascular compression of trigeminal nerve
Secondary - multiple sclerosis, space occupying lesion, skull-base bone deformity, connective tissue disease, arteriovenous malformation
Presentation of trigeminal neuralgia
Unilateral maxillary or mandibular division pain opthalmic division
Stabbing pain 5-10 secs duration
Triggers - cutaneous, wind, cold, touch, chewing
Purely paroxysmal or with concomitant continuous pain
Remissions and relapses
Trigeminal neuralgia on continuum with other cranial nerve pain disorders presentation
Acute spasms of sharp shooting pain
May be more than one division
May be bilateral
May have burning component
May have vasomotor component
Typical trigeminal neuralgia patient
USually older
Mask like face
Appearance of excrutiating pain
NO obvious precipitating pathology
Trigeminal neuralgia red flags
Younger <40
Sensory deficit in facial regions - hearing loss
Other cranial nerve lesions
ALWAYS test cranial nerves
All patients now get MRI
First line drug therapy for trigeminal neuralgia
Carbamazepine
Oxycarbazepine
Lamotrigine (slow onset of action)
Second line drug therapy for trigeminal neuralgia
Gabapentin
Pregabalin
Phenytoin
Baclofen
Carbamazepine side effects
Blood dyscrasias - thrombocytopenia, neutropenia, pancytopenia
Electrolyte imbalances
Neurological deficits - paraesthesia, vestibular problems
Liver toxicity
Skin reactions
When to consider surgery for trigeminal neuralgia?
When approaching maximum tolerable medical management even if pain controlled
Younger patients with significant drug use - will have many years of drug use
Trigeminal neuralgia surgical options
Microvascular decompression
Steriotactic radiosurgery
Destructive central procedure
Destructive peripheral neurectomies
Complications after trigeminal neuralgia surgery
Sensory loss
Motor deficits
May be reversible or irreversible
Causes of painful trigeminal neuropathy
Herpes zoster virus
Trauma
Idiopathic
Painful trigeminal neuropathy characteristics
Pain is localised to the distribution of the trigeminal nerve
Commonly described as burning or squeezing/pins and needles
Primary pain continuous (or near)
Superimposed brief pain paroxysms
Cluster headache
Mainly orbital and temporal pain
Attacks strictly unilateral
Rapid onset
Duration 15m-3hours
Rapid cessation of pain
Excruciatingly severe
Premonitory tiredness/yawning
Associated nausea vomiting photophobia phonophobia aura
80-90%Cluster in bouts 1-3 months remission lasts 1 month+
1 every other day to 8 per day
10-20% chronic cluster >1 year remission <1month
Paroxysmal Hemicrania
Orbital and temporal pain
Strictly unilateral
Rapid onset
2-30 mins then rapid cessation
2-40 attacks per day
Excruciating
Absolute response to indometacin
80% chronic 20% episodic
Paroxysmal hemicrania drug therapy
No abortive treatment
Prophylaxis with indomethacin
Alternatives COX-II inhibitors, topiramate
