Oral ulceration Flashcards
define ulcer
lesion wherein there is a full thickness breach of the epithelial continuity mucosa leaving connective tissue exposed
what is it if there is not a full breach of epithelial continuity
it is erosion or abrasion
clinical appearance of an ulcer
yellow sloughing base with erythematous halo
types of ulcers
- Primary = direct formation of an ulcer (ie trauma)
- Secondary = ulcer tht commenced as another lesion eg blister/vesicle
what salient history details do you need for an ulcer? (9)
- recurrent / persistent
- nature of initial lesion
- time and sequence
- ulcer / blister
- age of onset - SCC usually age 60+
- extra-oral involvement (genitals, skin, scalp, nails)
- pain - controversial (white + pain = bad)
- medical / social history
- systemic disease / drug therapy
what do you look at in the examination of an ulcer? (10)
- Base (yellow, homogenous = fine, speckled, heterogenous = worry)
- granularity
- margin
- rolled
erythematous halo = aphthous - regularity of outline
- texture
- induration = hard = malignancy
- site and distribution
- associated features
causes of ulcers (7)
- Traumatic = mechanical/chemical/thermal
- drug induced
- idiopathic = recurrent aphthous stomatitis
- associated with systemic disease = Behcet’s/Crohn’s/Coeliac/Paget’s
- associated with dermatological diseases = LP, DLE, MMP, PV
- Infective = bacterial/viral/fungi
- Neoplastic = SCC - non healing ulcer
what is the most common cause of oral ulceration?
Traumatic ulcer caused by
- ill-fitting dentures
- orthodontic appliances
- sharp cusps
- self-induced
lip biting
aspirin burn
- erythema multiforme
what do long stading ulcers get
keratotic edges → raised + rough
what is a chronic traumatic ulcer
takes a while to heal → white halo
- Once identifying and removing cause, should take ~10days to heal
Treatment of traumatic ulcers (4)
Remove cause
Difflam spray (LA)
Keep clean (CHX)
Review – improvement should be seen in 2 weeks.
what drug’s can cause drug induced ulcers?
- Nicorandil (K-channel activator)
- NSAID’s (aspirin ibuprofen)
- Bisphosphonates (alendronate)
- SSRI (sertraline)
- Chemotherapy agents (methotrexate)
Nicroandil and drug induced ulcers
Nicorandil = K-channel activator
- used for heart problems
- vasodilators
- treatment for angina
- often affects palate
- normally seen with an increase in dose, not when first starting drug
management of drug-induced ulcer
CHX, review 2/52
What is the characteristic pattern of recurrence for recurrent aphthous stomatitis (RAS)?
History of recurrent oral ulcers in otherwise healthy person – lesions normally come and go (not constantly present)
What is the typical gender and age of onset for recurrent aphthous stomatitis (RAS)?
RAS has a slight female predominance and usually begins in childhood or adolescence
How does smoking influence recurrent aphthous stomatitis (RAS)?
RAS is uncommon in tobacco smokers. smokers have Hyperkeratotic mucosa which thins when they stop smoking, potentially leading to the development of RAS
What does RAS ulceration look like
- yellow base
- erythematous halo
- round/oval
- soft on palpation
Describe the typical appearance of a minor RAS ulcer
- Most common (80%)
- Non-keratinised mucosa
- 2-10 ulcers
- <1cm diameter
- Heal within 7-14 days
- No scarring
- Painful
How does major RAS differ from minor RAS in terms of ulceration and healing?
- Uncommon (10%)
- 1-3 ulcers
- > 1cm diameter
- Slow healing – 1-2 months
- Possible scarring
- Non-keratinised or keratinised mucosa
- Often on soft palate/ uvula
What is the appearance and behaviour of herpetiform RAS ulcers?
- Uncommon (10%)
- Non-keratinised and keratinised mucosa
- Multiple ulcers
- 1-2mm diameter
- Heal variably, may scar (can coalesce and get bigger, then scar)
- Mimic HSV, but H-RAS are primary ulcers but HSV are secondary ulcers formed from vesicles bursting.
How can you differentiate between herpes simplex virus (HSV) ulcers and herpetiform RAS ulcers?
HSV vesicles pop → ulcers
H-RAS has inflamed gums
HSV systemically unwell
What investigations might be conducted to assess recurrent aphthous stomatitis (RAS)?
- diet diary
- full blood cell count (Hb so anaemia testing)
- haematinics (ferritin, B12, red cell folate) – will be a lack of
- coeliac disease in pts > as RAS rare in this age
what are some common triggering factors for recurrent aphthous stomatitis (RAS)?
stress
trauma
certain foods
How is RAS diagnosed
by exclusion
how is recurrent aphthous stomatitis (RAS) managed?
- Correct underlying systemic problems if present
- Topical antimicrobials: CHX 0.2% mouthwash/1% gel, tetracycline mouthwash
- Topical anti-inflammatory: Difflam mw/spray
- Topical steroids: prednisolone mw, betnesol mw (less potent, tablets that dissolve as used as mouthwash), fluticasone propionate (more potent), clobetasol mw
- Systemic treatment
What is the recommended use for chlorhexidine mouthwash in treating RAS?
Chlorhexidine mouthwash (0.2%) is used as a rinse, with 10ml used twice daily for 1min. A 300ml bottle is typically prescribed.
How should benzydamine mouthwash (Difflam) be used?
Benzydamine mouthwash (0.15%) should be used by rinsing or gargling with 15 ml every 1.5 hours as needed. A 300 ml bottle is typically prescribed.
What is the dosage and application for benzydamine oromucosal spray (Difflam)?
Benzydamine oromucosal spray (0.15%) should be sprayed 4 times onto the affected area every 1.5 hours. A 30 ml bottle is typically prescribed.
What is Behcet’s disease and how does it present?
Multisystemic inflammatory autoimmune disorder predominated clinically by:
- recurrent oral ulceration
- recurrent genital ulceration
- uveitis
multisystemic Behcet’s disease
- Cardiovascular
- Skeletal (arthritis)
- Mucocutaneous - (painful red lesions, typically on legs)
- Neurological
- Gastrointestinal
- Ocular
Found in people who live along the silk road (esp high in Turkey)
Treatment of Behcet’s disease
- Multidisciplinary
- Systemic steroids
- Anti-TNF therapy (Biologics)
- Oral lesions: colchicine, topical steroids, topical antimicrobials
first signs of Crohn’s
First sign often oro-facial granulomatosis
aetiology of Crohn’s and where it affects
- Aetiology unknown, autoimmune (inflammatory bowel disease)
- Can affect any part of gastrointestinal tract
what is crohn’s characterised by
abdominal pain
diarrhoea
weight loss
oral signs of crohn’s
- Linear/aphthous ulcers
- Buccal cobblestoning
- Orofacial (eg lips) swelling – can do intralesional steroid injections (triamcinolone 10mg/ml) to decrease swelling → OFG - to reduce swelling Tacrolimus
- Angular cheilitis
- Tissue tagging
- Hyperplastic gingivitis (full thickness gingival hyperplasia)
- Perioral erythema
- Lip swelling leading to fissure ulcers
what can be seen on a biopsy for crohn’s
Granulomas
what is coeliac?
- Autoimmune disease triggered by gluten
- Can present any time in life
Coeliac symptoms
GI disturbances, steatorrhea, fatigue, oral ulceration
Which antibody is commonly present in patients with Coeliac disease
tTGA (anti-tissue transglutaminase antibody)
What does a biopsy of the duodenum show in coeliac disease?
Biopsy of duodenum shows flattening of villi → malabsorption
What is the treatment for coeliac disease
lifelong gluten-free diet
What is lichen planus
Common chronic dermatological disease involving skin and mucous membranes (oral/genital mucosa, skin, scalp, nails)
Who is lichen planus most likely to affect?
F>M, middle aged patients, uncommon in children
what can clinically be seen with lichen planus
can be removed by scrapping
Aetiology of lichen planus
Unknown aetiology (immunopathogenesis) →
Chronic T cell mediated autoimmune mucocutaneous disease
what lesions do you get with lichen planus
extraoral and intraoral lesions
what t=do the extraoral lesions in lichen planus present like
pruritic purple papules on skin (3 P’s)
what do the intraoral lesions in lichen planus present like
Wickham’s striae mostly in buccal mucosa, also in other sites but uncommon in floor of mouth
what systemic diseases are associated with lichen planus
- liver disease
- graft vs host disease
- immunodeficiency
- diabetes/hypertension
what can cause lichenoid reactions?
- Dental materials: amalgam, composite
- Antimalarias: chloroquine
- Antihypertensives: metildopa, captopril, enalapril, propanalol
- NSAIDs: ibuprofen
- PANDDA → penicillin, antimalarials, NSAIDs, diuretics, dental materials, Antihypertensives
Histology of Lichen planus
Hey, I blame lichen planus
- Hyperparakeratosis
- Irregular acanthosis → some aread thick, some areas thin → saw-tooth rete ridges
- Band-like lympho-histiocytic infiltrate
- liquefaction of the basal cell layer
- presence of civatte bodies - hyaline bodies
types of lichen planus
- reticular = lace-like
- atrophic = diffuse red lesions
- plaque-like = white patches (close monitoring, can have malignant transformation)
- papular = small white patches
- erosive = extensive areas with ulceration
- bullous =subepithelial bullae
chance of malignant transformation in lichen planus?
0.1-2% malignant transformation → especially erosive / atrophic + plaque like
treatment of lichen planus
- identify and remove potential causes
- symptomatic relief - difflam mw spray
- topical steroids - prednisolone, betamethasone, fluticasone propionate (flixonase)
topical immunosuppressants (tacrolimus 0.1% to start then down to 0.03%) - systemic immunosuppressants - prednisolone, axathioprine, dapsone
what is pemphigus
Autoimmune reaction against desmosomes (anti-desmoglein 3) - holding cells together
who gets pemphigus
Rare childhood/early manifestations in adults
outcome of pemphigus if untreated
Fatal if untreated – extensive ulceration, electrolyte loss and infection
where does pemphigus usually present first
Frequently in mouth first due to subject to trauma
- Fragile bullae – rupture to form irregular, ragged, superficial ulcers
- Slow healing without scarring
- Severe desquamative gingivitis
- Soft palate, buccal mucosa and lips most common
what confirms pemphigus
Positive Nikolsky’s sign = look at rubbed surfaces now instead – upper epithelial layer sheds with little trauma
pemphigus histology
Histology – Teeny Tiny Little Blisters Ahhh
- Thin-roofed vesicles/bullae followed by ulceration
- Tzanck cells (acantholytic prickle cells) in blister fluid – swollen, hyperchromatic nucleus
- Little inflammatory infiltration until ulceration
- Basal cells remain attached (tombstone appearance)
- Acantholysis + destruction of desmosomes → suprabasal split
how is immunofluorescence used to diagnose pemphigus
- IgG and C3 intercellularly, incubate with fluoresceine
- Direct method = biopsy
- Indirect method = blood sample for fragile bullae
- Pemphigus = fluorescence show net-like pattern in epithelium
- Pemphigoid = fluorescence in basement membrane
Treatment of pemphigus
systemic corticosteroids + steroid-sparing agents (methotrexate, omalizumab, ciclosporin), immunosuppressive agents
what is mucous membrane pemphigoid (cicatricial pemphigoid)
Hemidesmosomes: separation from basement membrane
which area is almost always involved in mucous membrane pemphigoid (cicatricial pemphigoid)
Mouth almost always affected, sometimes only one side (oral pemphigoid)
what is the typical demographic affected by mucous membrane pemphigoid?
normally females over the age of 50
how do the bullae in mucous membrane pemphigoid differ from those in pemphigus?
they are occasionally hemorrhagic and tense, unlike in pemphigus
what are the common symptoms after the bullae rupture in mucous membrane pemphigoid?
rupture quickly, soreness, bleeding, and pain, with ulcerations healing slowly
what serious complication can result from ulceration of the conjunctiva in mucous membrane pemphigoid?
scarring on the conjunctiva, (cicatricial) ulceration of eyeball which can lead to blindness
what percentage of mucous membrane pemphigoid cases affect the gingiva, and what condition does it cause?
90%, causing desquamative gingivitis
besides the oral cavity, which other areas can be affected by mucous membrane pemphigoid?
ocular, nasal, larynx, pharynx, oesophagus, and genital areas
what histological feature characterises mucous membrane pemphigoid?
separation of the epithelium from the lamina propria, forming a bulla with a “thick roof”
what cellular infiltrations are observed as vesicles develop in mucous membrane pemphigoid?
Infiltration by neutrophils, eosinophils, and perivascular infiltration mainly by lymphocytes
how do we manage vesiculo-bullous disroders and desquamative gingivitis
- oral hygiene essential
- regular hygienist appointments
- avoid SLS toothpast
- topical steroids
what is desquamative gingivitis
- descriptive term, not a diagnosis
what does desquamative gingivitis look like
- shiny gingiva, smooth and thinned as a result of epithelial desquamation
- may involve free or attached gingiva
conditions which have desquamative gingivitis?
HomiPDL
- Hypersensitivity
- OLP (oral lichen planus)
- MMP (mucous membrane pemphigoid)
- (linear) IgA (linear IgA disease)
- PV (pemphigus vulgaris)
- DLE (discoid lupus erythematosus)
- LP again (lichen planus)
what is erythema multiforme
an acute blistering condition resulting in extensive shallow erosion, which may affect the oral mucosa alome or other mucosal sites, especially ocular and genital mucosa
what is the severe form of erythema multiforme called and why is it significant?
Stevens-Johnson Syndrome: it can occasionally be life threatening
What is the suspected immunological mechanism behind erythema multiforme?
it probably represents a type 3 hypersensitivity reaction (immune complex mediated)
What are the common symptoms of erythema multiforme?
the condition is typically recurrent and may mimic primary herpes, which can lead to diagnostic difficulties
What is a distinctive cutaneous feature of erythema multiforme?
the presence of “target” lesions on the skin
What are the possible causes of erythema multiforme?
- drug reactions (e.g. penicillin, trimethoprim, cotrimoxazole, aspirin, alcohol)
- Herpes simplex
- mycoplasma pneumoniae
What is a common but often unsatisfactory treatment for erythema multiforme?
systemic steroids , such as acyclovir
can erythema multiforme affect only one type of mucosal site?
Yes, it may affect the oral mucosa alone or involve other mucosal sites as well
What are the two types of viruses associated with herpetic stomatitis or primary gingivostomatitis?
HSV-1 and HSV-2 (herpes simplex virus types 1 and 2)
What percentage of people are infected with herpes simplex virus, and how many experience recurrent infections?
80% of people are infected, and 1/3 of them experience recurrent infections
How is herpetic stomatitis typically spread, and who is most commonly affected?
It is spread through contact or droplets and is most common in children (rarely under 6 years old) and young adults
what are the possible presentations or primary herpetic gingivostomatitis?
It can present as subclinical or mild pharyngitis, or symptomatic gingivostomatitis
what are the prodromal symptoms of gingivostomatitis and how long is the incubation period
The incubation period is approximately 5 days. Prodromal symptoms include malaise, fever, irritability, headaches, pain while swallowing, and regional lymphadenopathy
what happens after 1-2 days of prodromal symptoms in gingivostomatitis?
numerous vesicles appear on the mucosa and lips, which typically resolve within 2 weeks
What happens to the vesicles that form during herpetic stomatitis?
The vesicles ulcerate, may become secondarily infected, leading to regional lymphadenitis, and crust over with coagulated serum
What are the potential extra-oral lesions associated with herpetic stomatitis?
- drooling = lesions on the chin
- finger sucking = herpetic whitlow
- rubbing eyes = herpetic keratosis, which can lead to blindness if not treated with antiviral medication
how long is herpetic stomatitis considered infective?
until all the lesions have disappeared
What is the primary infection caused by the Varicella Zoster Virus (VZV)?
Chickenpox, characterised by small blisters and ulcers that can appear in the oral mucosa and palate, preceding the skin rash
What is the reactivation of varicella zoster virus known as?
Herpes-zoster, commonly known as shingles
how does Herpes-zoster typically present on the body?
It infects only one side of the body (unilateral)
What causes the reactiveness of VZV leading to shingles?
A decrease in host resistance allows the latent virus in sensory ganglia to reactivate
What are the initial symptoms of Herpes-zoster and what follows?
Prodromal symptoms are followed by unilateral vesicle eruptions that are painful and rupture, leaving ulcerated areas
which division of the trigeminal nerve is most commonly involved in Herpes-zoster?
The ophthalmic division more often
What is post-herpetic neuralgia?
A sequela of Herpes-zoster, where sensory nerves become fibrosed, causing pain that persists for more than 3 months
What type of pain is associated with post-herpetic neuralgia, and how is it managed?
Severe burning or electric shock-like pain in dermatomes supplied by the trigeminal nerve. It is managed with carbamazepine or Amitriptyline
What is Ramsey-Hunt syndrome, and what causes it?
A complication of VZV characterised by inflammation of the geniculate ganglion of the facial nerve
what are the clinical features of Ramsey-Hunt syndrome?
Unilateral facial paralysis, loss of taste, oral ulceration, external ear neuralgia, tinnitus, and vertigo
What causes measles?
The paramyxovirus
How was measles described in the pre-vaccination era, and where is it still a significant issue?
It was universal and highly contagious, often fatal in developing areas
What are the prodromal symptoms of measles?
Symptoms resemble a common cold and include the presence of Koplik’s spots
What are Koplik’s spots, and where are they found?
Small white or blue spots on the buccal mucosa, opposite the molar teeth
When do Koplik’s spots appear and disappear in the course of Measles?
They appear before the skin rash develops and disappear after the rash appears
What are the other diseases caused by the paramyxovirus family?
- Newcastle disease
- Parainfluenza (4 types)
- Mumps
What are the two common conditions caused by Coxsackie Type A virus?
Herpangina and Hand, Foot and mouth disease
Who is most commonly affected by Herpangina?
Children
What are the symptoms of Herpangina?
Sore throat, dysphagia, fever, headaches, vomiting, and abdominal pain, mouth blisters
What is the incubation period for Herpangina?
approximately 4 days
Describe the appearance and location of the vesicles in Herpangina
Small vesicles (1-2mm) on the tonsils, soft palate, and uvula, which ulcerate to form lesions with a grey base and inflamed periphery
How long does Herpangina typically last, and what is its nature?
It is self-limiting and typically resolves in about 7 days
How is the location of lesions in Herpangina different from those in herpes simplex virus (HSV) infection?
Herpagina affects the oropharynx, while HSV causes gingivostomatitis
Who is most commonly afffected by Hand, Foot and mouth disease
Young children
What are the typical clinical features of Hand, Foot and mouth disease?
Multiple ulcero-vesicular lesions on the hard palate, tongue, buccal mucosa, and skin.
What is the incubation period for Hand, Foot and Mouth Disease?
3-6 days
How long is Hand, Foot and mouth disease infectious, and when does the contagious period end
It is infective until the rash has disappeared
What is the typical duration and severity of Hand, Foot and Mouth disease?
It is mild, self limiting condition that usually lasts 5-7 days.
What is the primary lesion of syphillis called, and where is it typically located?
The primary lesion is called a chancre, typically found on the genitalia, but it can also appear on the oral mucosa or lips
What are the characteristics of a primary syphilis chancre?
A shallow, painless ulcer with an indurated base and associated lymphadenopathy
How long does it take for a primary syphilis chancre to heal spontaneously?
3-6 weeks
What are the main features of the secondary phase of syphilis?
Generalised skin rash, mucous patches, and ulceration that may coalesce into “small track” lesions
When does the secondary phase of syphilis typically appear?
2-3 months after the intial infection
What is the main characteristic of tertiary sypilis?
Formation of gummas, which are areas of coagulative necrosis and granulation tissue that can cause palate perforation
What is a serious complication associated with the white lesions in tertiary syphilis?
An increased risk of oral squamous cell carcinoma (OSCC)
What are the dental anomalies associated with congenital syphilis?
Hutchinson’s incisors and mulberry molars
How does syphillis affect the feotus if the mother is infected during pregnancy?
It affects the second germ layer, leading to congenital syphilis
What is the characteristic oral lesion of tuberculosis?
A solitary ulcer, often found on the underside of the tongue
How is the ulcer in tuberculosis typically described
as a non-specific ulceration
