Oral Medicine Flashcards
1
Q
How is oral ulceration managed?
A
Nutritional deficiencies
Avoid sharp or spicy foods
Prevention of superinfection
Symptomatic relieve
2
Q
What are Bohn’s Nodules?
A
Gingival cysts filled with keratin in the alveolar ridge
3
Q
What are fibro-epithelial polyps?
A
Localised hyperplastic lesion
4
Q
What is the aetiology of fibro-epithelial polyps?
A
Overproduction of granulation and fibrous tissue in response to damage or trauma
5
Q
What are the clinical features of fibro-epithelial polyps?
A
Pedunculated or sessile
Firm or soft
Pink appearance
Painless
Can be ulcerated and easily traumatic
May have associated frictional keratosis
Usually an isolated lesion
6
Q
Where do fibro-epithelial polyps present?
A
Buccal mucosa
Areas of trauma
7
Q
Describe the histology of a fibre-epithelial polyp:
A
Fibrous core
Thick interlacing collagen
Adjacent normal tissue
Covered with squamous epithelium
May have hyperkeratosis
Little inflammatory infiltrate
8
Q
What are the clinical considerations in regard to fibro-epithelial polyps?
A
Does it bother the patient?
Do they have risk factors for oral cancer?
9
Q
What is the name for a fibro-epithelial polyp on the gingiva?
A
Fibrous epulis
10
Q
What is the management of a fibro-epithelial polyp?
A
Photos
Identify and if appropriate, correct the traumatic cause
Consider excision biopsy
11
Q
What are the benefits of excision biopsy for fibro-epithelial polyps?
A
Can confirm diagnoses
Can remove the lesion
12
Q
What are the risks of excision for fibro-epithelial polyps?
A
Surgical risks
Altered sensation- can be permanent
Recurrence or incomplete excision
13
Q
What are examples of hyperplasticity tissue conditions related to dentures?
A
Leaf fibroma
Denture hyperplasia
Papillary hyperplasia
14
Q
What is papillary hyperplasia?
A
Granular inflammation of denture bearing surface- more common on palate
15
Q
What is papillary hyperplasia associated with?
A
Candida
16
Q
What is the management for denture associated lesions?
A
Consider excision of lesion
Denture hygiene
Candida management
Consider making a new prosthesis
17
Q
What is an epulis?
A
A reactive hyperplastic lesion on the gingiva
18
Q
What are the features of fibrous epulis?
A
Fibro-epithelial polyp on the gingiva
Same colour as gingiva
May be ulcerated
19
Q
What is giant cell epulis also known as?
A
Peripheral giant cell granuloma
20
Q
Describe the presentation of giant cell epulis:
A
Red/purple appearance
Sessile or pedunculated
Often interdental
Most common in children
21
Q
What does giant cell epulis have identical histopathological features as?
A
Central giant cell lesion
Hyperparathyroidism (Brown’s Tumour)
22
Q
What is the histopathological presentation of giant cell epulis?
A
Multi-nucleated osteoclast giant cells
Vascular stroma
Fibrous tissue
23
Q
What is the pathogenesis of giant cell epulis?
A
Unknown
Reactive to trauma or irritation
24
Q
What is the management of giant cell epulis?
A
Excisional biopsy
OPT +/- CBCT
Bone profile
Parathyroid hormone assay
Photos and investigation from paeds clinic
25
What is a vascular epulis the same as?
Pyogenic granuloma
26
What is the name of a vascular epulis that presents in pregnancy?
Pregnancy epulis
27
Why do pregnancy epulis present/increase in size?
Hormonal changes- may resolve following birth and result in a fibrous epulis
May recur if removed during pregnancy
28
What is the presentation of a vascular epulis?
Soft-bright red appearance
Gradual increase in size
29
What is the histological appearance of a vascular epulis?
Vascular appearance
Variable amounts of inflammatory infiltrate
30
What are the management options for a vascular epulis?
Keep under observation
Refer to oral surgery in GDP
Excisional biopsy
Excise after birth (pregancy epulis)
31
What drugs are associated with generalised gingival overgrowth?
Calcium channel blockers
Ciclosporin
Phenytoin
32
What is the management of gingival overgrowth?
Gingivoplasty
Ask GP to consider alternative medications
Plaque control
Are there risk factors for other disease
Consider referral to Oral Medicine to exclude other causes
33
What is chronic hyperplastic gingivitis associated with?
Mouth breathing
Pregnancy
34
How does hereditary gingival fibromatosis present?
Enlarged gingiva
Little inflammation
Expansion of the tuberosities
35
What is a sign of haematological malignancy associated with gingival overgrowth?
Rapid progression in presence of good OH
36
What is squamous cell papilloma also referred to as?
Benign growth (tumpur)
Wart
37
How does squamous cell papilloma present?
Pedunculated or sessile
Cauliflower appearance
Often keratinised surface
Single or multiple lesions
38
What is the aetiology of squamous cell papilloma?
Viral- HPV infection (HPV: 2,4,6,11 and 40)
May present in immunocompromised
39
What is the management of squamous cell papilloma?
Excisional biopsy
Observation: if no red flag signs, symptoms or OSCC risk factors
40
What is the histological presentation of squamous cell papilloma?
Finger like processes of hyperplastic squamous epithelium
Thin cores of vascular connective tissue
41
What is a pyogenic granuloma?
Reactive vascular lesion
42
Where do pyogenic granulomas present?
Gingiva usually
43
What is the cause of pyogenic granulomas?
Response to local irritation/trauma
44
What is the histological presentation of a pyogenic granuloma?
Vascular proliferation
Oedematous fibrous stroma
Variable inflammatory infiltrate
45
What is the management of pyogenic granulomas?
Remove irritant- plaque/overhangs/denture/trauma
Excisional biopsy
Photos
46
What is the pathophysiology of black hairy tongue?
Hyperplasia of filiform papillae
Build up of commensal bacteria, food debris
Pigment inducing fungi and bacteria
47
What are factors associated with the development of black hairy tongue?
Smoking
Antibiotics
Chlorhexidine mouthwash
Poor oral hygiene
48
What is the management of black hairy tongue?
Re-assure
Stop smoking
Stay hydrated
Lightly brush the tongue
Gently exfoliate tongue surfaces- peach stones
Eating fresh pineapple
49
What are fordyce spots?
Sebaceous glands
50
What do fordyce spots present as:
Yellowish bumps on the buccal mucosa and lips
Symmetrical distribution
Greater prominence later in life
51
What % of adults have fordyce spots?
60-75%
52
What is geographic tongue also called?
Benign migratory glossitis
Erythema migrans
53
What % of adults have geographic tongue?
1-3%
54
What is geographic tongue associated with?
Psoriasis
55
What is geographic tongue?
Loss of filiform papillae- areas of tongue atrophy and hyper keratinisation
56
What are the symptoms of geographic tongue?
Asymptomatic
Sensitivity to hot and spicy foods and toothpaste
57
What is the management of geographic tongue?
Reassurance
Biopsy not indicated
If symptomatic- consider difflam mouthwash
Ask about skin changes (psoriasis)
Consider avoiding trigger foods if painful
58
What are mucoceles?
Cysts
59
What are mucoceles caused by?
Damage to salivary ducts or minor salivary glands
60
What is a ranula?
Mucocele on floor of mouth
61
Where do mucoceles present?
Lower lip mainly
If upper lip- treat as malignancy until proven otherwise
62
How do mucoceles present?
Blue/translucent lump
Sessile
63
How are mucoceles classified?
Mucous retentive
Mucous extravasation
64
What age group are mucoceles most common in?
Under 30
65
What is the management of mucoceles?
Excision- blunt dissection to remove full capsule of cyst and damaged minor salivary gland
Paeds- watchful wait
66
What happens if a mucocele is incompletely excised?
Increased chance of reoccurrence
67
What is a lingual tonsil?
Lymphoid tissue
68
Where is a lingual tonsil found?
Postero-lateral aspect of tongue
69
What is a varice?
Blood vessel
70
When are varices more prominent?
Increasing age
Smokers
CVD patients
71
What is a hamartoma?
Disorganised vascular tissue
72
Where do hamartomas present?
Head and neck
73
What is a haemangioma?
Common, benign growth made of a collection of small blood vessels that form a lump under the skin
74
What are the histological subtypes of haemangioma?
Capillary- smaller capillary vessels
Cavernous- large thin walled vessels
75
What groups are haemangiomas most common in?
Children
Females
76
What is a vascular malformation?
Congenital lesion due to abnormal blood vessel development
77
What are vascular malformations associated with?
Larger arteries and veins
Stuge-weber syndrome
78
When do vascular malformations present?
Birth
Different times of life
79
What is the management of vascular malformations?
No treatment
Ultrasound
Cryotherapy
Cauterisation
MRI +/- Angiogram (large lesions)
May require extensive excision and free-flap reconstruction
80
What is the histological presentation of tori and exostoses?
Thicker epithelium
Broad rete process
81
What is linea alba?
Horizontal, asymptomatic white lesion along the occlusal
82
What is the histological appearance of linea alba?
Parakeratosis
Prominent or reduced granular layer
Acanthuses
83
What is fissured tongue?
Variation of normal anatomy
Occurs later in life
No treatment needed
Associated with geographic tongue
84
What is the management of fissured tongue?
Encourage good oral hygiene
Consider lightly brushing tongue
85
What is a bony exostosis?
Usually benign overgrowth of calcified bone
Associated with parafunction
86
What % of the population have bony exostosis?
30-40%
87
Where do bony exostosis present?
Palate: torus palatinus
Mandible: torus mandibularis (typically lingual)
88
What is the management of bony exostosis?
Monitoring: photos, study models, x-rays
89
What should be considered with patients with physiological pigmentation?
Addisons disease
Smokers melanosis
Drug-related pigmentation
90
What are the systemic risk factors for oral candida infection?
Immunocompromised: medication, medical conditions
Deficiency states: anaemia
Extremes of age
91
What are the local factor that influence oral immunity or ecology and are associated with increased oral candida infection risk?
Hyposalivation
Smoking
Broad-spectrum antimicrobials
Corticosteroids
Dental appliances
Irradiation involving the mouth or salivary glands
92
What is candida infection also known as?
Thrush/Yeast/Fungal infection
93
What is the management of oral candidiasis?
Antifungal therapy
Local measures
Investigations to exclude systemic disease
94
What anti fungal therapy can be provided to patients with oral candida?
Fluconazole
Miconazole
Nystatin
95
What local measures of management can be provided to patients with oral candida?
Rinse after inhalers
Use a spacer
Denture hygiene
Smoking cessation
96
What is traumatic keratosis?
Increased keratin deposition at a site of trauma
Protective response
97
What is the management of traumatic keratosis?
Encourage smoking cessation
Take photographs
98
What are the six types of oral lichen planus and oral lichenoid reactions?
Reticular
Atrophic
Papular
Erosive
Plaque like
Bullous
99
What is oral lichen planus?
CD8+ T Cell mediated destruction of basal keratinocytes
Chronic inflammatory condition
100
How does oral lichen planus present?
Asymptomatic or burning/stinging sensation
101
What is the difference between oral lichen planus and oral lichenoid tissue reactions?
Oral lichen planus is generalised and idiopathic
Oral lichenoid tissue reactions are localised and may be a response to medicines/allergens
102
What is the malignant potential of oral lichenoid reactions?
1% over 10 years
103
What should you ask a patient with oral lichen planus/oral lichenoid reactions about?
Systemic symptoms or recent cancer therapy
104
What drugs can cause oral lichenoid reactions?
Antihypertensives
Antimalarials
NSAIDs
Allopurinol
Lithium
105
What materials can cause oral lichenoid reactions?
Metals (gold, nickel)
Composite resin
106
What is the management of oral lichen planus/ oral lichenoid reactions?
1. Simple mouthwash (HSMW)
2. Local anaesthetic (Benzydamine or lidocaine)
3. Avoid trigger factors (spicy foods, fizzy drinks)
4. Steroid mouthwash (Betamethasone MW, Beclometasone inhaler or hydrocortisone oromucosal tablets
5. Change restorations (composite causative?)
6. Onward referral- biopsy, inform of increased cancer risk, stop the cause
107
What is hairy leukoplakia?
Non-removable white patch
Acanthotic and para-keratinised tissue
Finger-like projections of para keratin
108
Where is hairy leukoplakia usually?
Lateral borders of tongue
109
What are the risk factors for hairy leukoplakia?
Triggered by EBV
Immunocompromised
110
What % of HIV patients have hairy leukoplakia?
20-25%
111
What is leukoplakia?
Diagnosis of exclusion
No obvious cause for white patch
Has malignant potential
Can be dysplastic: group of abnormal cellular changes associated with malignancy
112
What is a red patch with no clear cause associated with?
A high likelihood of being dysplastic or malignant
113
What is granulomatosis with polyangitis also known as?
Wegner's granulomatosis
114
What is granulomatosis with polyangitis?
Systemic vasculitis
May present with fever and weight loss
115
How is granulomatosis with polyangitis managed?
Immunosuppressants
116
What % of patients with granulomatosis with polyangitis have ear, nose or throat manifestations?
92%
117
What is erythroplakia?
Velvety, fiery, red patch
High malignant transformation
118
How is erythroplakia diagnosed?
Diagnosis of exclusion
119
What is the management of erythroplakia?
Urgent referral (high malignant transformation)
Consider urgent biopsy for histopathology
120
What is OFG and Oral Crohn's?
Non-necrotising granuloma formation
121
What is the management of OFG and Oral Crohn's?
Topical steroids
Avoidance diets
Intralesional steroid
Biologics for crohns disease
Infliximab, adalimumab (anti TNF), ustekinumab (Anti IL21/23), Vedolizumab (Anti-a4b7)
122
123
How many oral cancer cases are diagnosed per year?
500
124
What is the % survival for an early diagnosis of oral cancer?
50%
125
What is the % diagnosis for a late diagnosis oral cancer?
50%
126
What are the red flags for oral cancer?
>3 week duration
>50 years old
Smoking
High alcohol consumption
History of oral cancer
Non-homogenous
Non-healing ulceration (with no cause)
Indicated
Exophytic
Tethering of tissue
Tooth mobility
Non-healing extraction sockets
Difficulty speaking/swallowing
Cervical lymphadenopathy
Weight loss/appetite loss
Numbness/altered sensation
127
How can we increase early detection?
Soft tissue exam for every patient
Patient education and empowerment
Recognition of complex social, cultural, public health reasons behind risk behaviours, poor attendance and access to dental practices
128
What are the risk factors of oral cancer?
Smoking
Poor OH
HPV
Alcohol
Chewing tobacco/betel/areca nut
Socio-economic background
Low fruit/veg
129
What is oral epithelial dysplasia?
Abnormal growth
130
How is oral epithelial dysplasia diagnosed ?
By histology
131
What are the risk factors of oral epithelium dysplasia?
Smoking
Alcohol
HPV
Genetics
132
How does Oral epithelium dysplasia present?
Patches of red/white
133
What are the four factors of describing lesions?
Site
Size
Colour
Texture
134
What is a higher risk site of an oral lesion?
Ventrolateral tongue and FoM
135
What should you look at when considering the texture of a lesion?
Can you feel it when palpating?
Is it thickened/rough/corrugated/firm/rubbery?
136
What should you look at when considering the texture of a lesion?
Can you feel it when palpating?
137
What are the architectural features of oral epithelial dysplasia?
Irregular epithelial stratification
Loss of polarity of basal cells
Drop-shaped rete ridges
Increased number of mitotic figures
Abnormally superficial mitoses
Premature keratinisation in single cells (dyskeratosis)
Keratin pearls with rete ridges
Loss of epithelial cell cohesion
138
What are the cytological features of oral epithelial dysplasia?
Abnormal variation in nuclear size
Abnormal variation in nuclear shape
Abnormal variation in cell size
Abnormal variation in cell shape
Increased nuclear-cytoplasmic ratio
Atypical mitotic figures
Increased number and size of nucleoli
Hyperchromasia
139
What are the molecular markers for Oral Epithelial Dysplasia?
Signalling pathways: EGFR
Cell cycle: Ki67, p53, pRB
Immortalisation: Telomerase
Apoptosis: p53, p21
Angiogenesis: VEGF
COX-1&2 enzymes
Proliferation and differentiation markers
Viruse: HPV + and HPV-
Loss of heterozygosity (LOH): 3p, 9p, 13q (retinoblastoma), 17p
140
How does basal hyperplasia present?
Increased basal cell numbers
Regular stratification and basal compartment is larger (architecture)
No cellular atypia
141
How does mild dysplasia present?
Architecture; changes in the lower third
Cytology: mild atyppia
Pleomorphism, hyperchromatism
142
How does moderate dysplasia present?
Architecture: change extends into the middle third
Cytology: moderate atypia
143
How does severe dysplasia present?
Architecture: changes extend to the upper third
Cytology: several atypia and numerous mitoses, abnormally high
144
How does carcinoma in situ present?
Malignant but not invasive:
Architecture: Abnormal, full thickness (or almost full) of viable cells
Cytology: pronounce cytological atypia- mitotic abnormalities frequent
145
How is oral epithelial dysplasia managed?
Mild or low grade- monitored (minimum 5 years)
Moderate or severe/high grade- considered for removal by OMS
146
What is the definition of oral potentially malignant disorders?
Any mucosal abnormality that is associated with statistically increased risk of developing oral cancer
147
What are examples of oral potentially malignant disorders?
Leukoplakia
Proliferative verracous leukoplakia
Erythroplakia
Oral submucous fibrosis
Oral lichen planus
Oral lichenoid lesion
Actinic cheilitis/keratosis
Palatal lesions in reverse smokers
Oral lupus erythematosus
Dyskeratosis congenital
Oral graft vs host disease
148
What is the definition of leukoplakia?
Predominantly white patch, not attributed to another disorder
149
What are the two types of leukoplakia?
Homogenous- typically well demarcated
Non-homogenous- diffuse borders, red/nodular components
150
What could leukoplakia be?
Frictional keratosis
Biting habits
Oral lichen planus
Pseudomemranous candidiasis (can be scraped off)
Leukoedema (bilateral, disappears on stretching)
Nicotinic stomatitis
Papilloma
151
What is proliferative Verrucous leukoplakia?
Distinct form of multi-focal oral leukoplakia
Progressive
152
What Oral potentially malignant condition has the highest risk of malignant change?
Proliferative verrucous leukoplakia
153
What is erythoplakia?
Predominantly fiery red patch that cannot be characterised clinically or pathologically as any other definable disease
Solitary lesion, typically well demarcated
154
What can distinguish erythroplakia from widespread conditions?
Solitary nature
155
What is oral submucous fibrosis?
Progressive condition leading to the loss of elasticity which progresses to fibrosis of the lamina propria
Function limiting
156
What may a patient with oral submucous fibrosis present with?
Burning sensation with spicy food
Later restricted mouth opening
157
What habits are associated with oral submucous fibrosis?
Paan- areca nuts, slaked lime, betel leaves
158
What is oral lichen planus?
Inflammatory condition of the oral mucosa,
Usually Idiopathic
159
What does erosive oral lichen planus lead to?
Ulceration and erthemaotous erosions
160
What do oral lichenoid lesions include?
Atypical OLP/unilateral lesions
Lichenoid tissue reactions
Lichenoid drug reactions
161
What factors are considered in regard to risk vs benefit of removing amalgam restorations in oral lichenoid lesions
Potential for tooth to become symptomatic
Requiring larger restoration
Requiring crown
Unrestorable
No resolution
162
What is actinic cheilitis?
Diffuse, patch with dryness and thickening associated with solar radiation exposure
163
How is actinic cheilitis prevented?
Smoking cessation
UV protection
164
What is often the cause of a palatal lesion in a reverse smoker?
Burning end of cigarette held in mouth
165
What is dyskeratosis congénita?
Rare hereditary condition
Leukoplakia and hyperpigmentation of skin and nail dystrophy
166
What is oral systemic erythematosus?
Autoimmune inflammatory condition
Clinically similar to OLP- starburst appearance on hard palate
167
What % of systemic lupus erythematosus have oral lesions?
20%
168
What is an example of a previously included oral potentially malignant disorder?
Chronic hyperplasticity candidiasis
169
What is chronic hyperplastic candidiasis?
Occurs in smokers
170
What is the treatment of chronic hyperplastic candidiasis?
Antifungal treatment
171
What are the causes of oral ulcers?
Trauma
Metabolic/nutritional
Allergic/hypersensitive
Infective
Inflammatory
Immunological
Drug Induced (iatrogenic)
Neoplastic
Idiopathic
172
What factors should be considered when assessing the aetiology of an ulcer?
Site
Onset
Duration
Number
Texture
Appearance
Size
Pain
Predisposing factors
Relieving factors
173
How does a traumatic ulcer present?
White (keratotic) borders
Clear causative agent
Surrounding mucosa normal and ulcer soft
174
What is the most common ulcerative condition?
Aphthous ulcers
175
How does an aphthous ulcer present?
Painful
Red border
Yellow/white centre
176
What % of the population experience aphthous ulcers?
20%
177
How does a major recurrent aphthous ulcer present?
Greater than 1cm
Long time to heal
178
How does a minor recurrent aphthous ulcer present?
Less than 1cm
Heals in 2-3 weeks
179
How does a herpetiform recurrent aphthous ulcer present?
Multiple small ulcers that may coalesce
180
What are the triggers for aphthous ulcers?
Stress
Trauma
Allergy
Sensitivity
181
What are the metabolic/nutritional causes of ulcers?
Associated with growth in children/teens
Adults with occult GI/GU pathology
Malnourishment
Anaemia
182
What are inflammatory/immunological causes of ulcers?
Behcet's
Necrotising sialometaplasia
Lichen planus ]
Vesiculobullous disease
Connective tissue disease
183
Where does behcet's affect?
Aphthous appearance ulcers on mouth, skin, genitals and eyes
184
What are examples of connective tissue diseases?
Systemic Lupus Erythematous
Rheumatoid Arthritis
Scleroderma
185
What questions should you ask when you suspect a GIT cause for ulcerations?
Abdominal pain
Post rectal blood/mucous
Altered bowel motions
Unintentional weight loss
186
What questions should you ask when you suspect a connective tissue disease cause for ulcerations?
Joint pain and stiffness
Photosensitive rashes
Xerophthalmia/xerostomia
Fatigue
187
What are infective causes of ulceration?
Primary or recurrent herpes simplex virus infection
Varicella-zoster virus
Epstein-barr virus
Coxsackie virus
Echovirus
Treponema pallidum
Mycobacterium tuberculosis
Chronic mucocutaneous candidiasis
HIV
188
What age group is commonly affected by primary herpes simplex virus infection?
2-5 years
189
How does primary herpes simplex virus infection present systemically?
Fever
Headache
Malaise
Dysphagia
Cervical lymphadenopathy
190
How does primary herpes simplex virus infection present in the oral cavity?
Short lasting vesicles on the tongue, lips, buccal, palatal and gingival mucosa which then form ulcers
191
Explain the pathway of the varicella-zoster virus?
Primary varicella-zoster infection: Chicken Pox
Virus remains latent in sensory ganglion
Reacrivation of latent virus results in VCZ infection: Shingles
192
How does the varicella-zoster infection present?
Distributed over a dermatome
Reactivated due to immunocompromisation or acute infection
193
How are patients with varicella-zoster managed?
Lisa with GP
May need further investigations, provide analgesia and difflam if painful
194
What are iatrogenic causes of ulceration?
Chemotherapy
Radiotherapy
Graft vs Host disease
Drug Induced Ulceration
195
What drugs are associated with drug induced ulceration?
Potassium channel blockers
Bisphosphonates
NSAIDs
DMARDs
196
How do neoplastic ulcers present?
Exophytic
Rolled borders
Raised
Hard to touch
Non moveable
Not always painful
Sensory disturbance
197
What is the local management pathway of ulceration?
If suspicion of malignancy- refer to OMFS
Reverse the reversible
Refer to GP for FBC/Haemantics/Coeliac Screen (aphthous appearance)
1. Simple Mouthwash (HSMW)
2. Antiseptic mouthwash (hydrogen peroxide or CHX or doxycycline)
3. Local anaesthetic (Benzydamine spray or mouthwash)
4. Steroid mouthwash (betamethasone)
5. Steroid inhaler (beclometasone)
6. Onward referral
198
What are the three types of pain?
Nociceptive
Inflammatory
Pathological
199
What is the cause of pathological pain?
Abnormal functioning of the nervous system
200
What are the causes of mucosal non-odontogenic intra-oral pain?
Ulcers
Lichen planus
Vesticulobullous disorders
Salivary gland pain
201
What are the causes of non-odontogenic intra-oral pain?
Neuropathic pain
Trigeminal neuropathic pain
Persistent idiopathic dentoalveolar pain
202
What are examples of neuropathic pain?
Non-diseased dento-alveolar structure
Presents with burning/shooting/shot-like/allodynia/hyperalgesia
203
How does oral dysesthesia (burning mouth syndrome) present
Pain/burning sensation
Altered sensation ]
Perception of dry or excess saliva
204
What can cause trigeminal neuralgia?
Tumour
MS
Neurovascular conflict
205
How does trigeminal neuralgia present?
Electric shock/shooting/stabbing
Unilateral
Severe 10/10
Short lasting
Episodic
206
How should you manage suspected trigeminal neuralgia?
MRI
207
Why do oral lesions appear white?
The epithelium has thickened
208
What conditions are associated with white lesions?
Congenital
Lichen Planus
Infections
Neoplastic/potentially neoplastic
Keratosis
209
What are organic material causes of white lesions?
Candida infection
Food debris
210
What are physiological causes of white lesions?
Tongue coating
Desquamation
Leukoedema
211
How does leukoedema present?
Faint white lines (typically buccal mucosa)
Fade or disappear on starching mucosa
212
What ethnicity is leukoedema common in?
African heritage
213
What are the genetic associations with White Sponge Naevus?
Inherited Autosomal dominant
Mutation of genes that code for keratins 4 and 13
214
How does white sponge naevus present?
Affects oral mucosa (commonly buccal)
Presents in adolescence or childhood
Poorly defined border
Benign
215
What is the histology of white sponge naevus?
Acanthotic- thickening of epithelium (especially stratum spinosum)
Hyperkeratosis
Intra-cellular oedema in stratum spinosum and parakeratinised layers
No inflammatory changes
216
How does Darier disease present?
Rare autosomal dominant disorder
Hyperkeratosis papules affecting seborrheic areas on head, neck, skin folds and thorax
Crusted papules
Oral manifestations rare but affect palatal and alveolar mucosa
Asymptomatic
217
How does focal palmoplantar and oral mucosa hyperkeratosis syndrome present and genetic aspect?
Autosomal dominant
Affects soles, palms and oral mucosa- mainly keratinised tissue
Rare
218
What restorative materials are associated with lichen planus and lichenoid tissue reactions?
Amalgam
Gold
Polymerised plastics
219
What medications are associated with lichen planus and lichenoid tissue reactions?
Anti-malarials
Oral hypoglycaemic
NSAIDs
220
What food and food additives are associated with lichen planus and lichenoid tissue reactions?
Flavouring- cinnamon and derivatives
221
How does hairy leukoplakia present?
Presents on lateral aspects of tongue
Bilateral
222
What are the causative factors of hairy leukoplakia?
EBV infection in immunocompromised; HIV (decreases CD4+ T cell count), diabetes, steroid use
223
What are examples of neoplastic and potentially malignant white patches?
Squamous cell carcinoma
Leukoplakia
Submucous fibrosis
Actinic Chelitis
224
What are the red flags associated with squamous cell carcinoma?
>3 week duration
>50 years old
Smoking
High alcohol consumption
History of oral cancer
Non-homogenous
Non-healing ulceration
Induration
Exophytic
Tethering of tissue
Tooth mobility
Non-healing extraction sockets
Difficulty speaking/swallowing
Cervical lymphadenopathy
Weightless/appetite loss/fatigue
Numbness/altered sensation
225
How is suspected squamous cell carcinoma managed?
Urgent cancer referral to oral and maxillofacial surgery
Follow local guidelines
Be honest with patient and explain concerns and that a biopsy should be taken promptly
226
How does homogenous leukoplakia present?
Uniformly white, flat and thin
Smooth surface
May exhibit shallow cracks
227
What is the definition of leukoplakia?
A white patch or plaque that cannot be characterised clinically or pathologically
Diagnosis of exclusion
Cannot be rubbed away
228
How does verrucous leukoplakia present?
Surface is raised, exophytic, wrinkled or corrugated
229
What % of leukoplakia will become malignant in ten years?
2-5%
230
What % of leukoplakias are displastic?
5-20%
231
What % of leukoplakia showing dysplasia progress to carcinoma in 10 years?
10-35%
232
What are the clinical features of a leukoplakia that is likely to become malignant?
>200mm2
Non-homogenous texture
Red or speckled colour
Sited on tongue/ FoM
Female
>50 years
Smoker
233
What are the histological features of a leukoplakia that is likely to become malignant?
Severe/high risk of dysplasia
HPV-16 +
Aneuploidy DNA content
Loss of heterozygosity (many genes involved)
234
What disorders should be excluded for a leukoplakia diagnosis?
Leukoedema
White sponge naevus
Frictional keratosis
Chemical injury
Acute pseudomembranous candidiasis
Hairy leukoplakia
Lichen planus (plaque like variant)
Lichenoid reaction
Discoid lupus erythematous
235
What % of proliferative verrocous leukoplakia undergo malignant transformation?
85%
236
How does proliferative verrucous leukoplakia present?
Warty surface with white/yellow appearance
Palate and gingiva common sites
Enlarge overtime
237
How does oral sub mucous fibrosis present?
Pale in colour
Firm to palpate
Fibrous band develops
Buccal mucosa and soft palate typically affected
Mouth opening diminishes overtime
238
What % of oral submucous fibrosis becomes malignant?
5%
239
What is the general management of oral potentially malignant disorders?
Smoking cessation
Increase fruit and veg intake
Mapping biopsies
Observation with clinical photos
Consider excision if evidence of dysplasia
Monitor
240
What is a keratose?
Response to trauma- frictional, thermal or chemical
241
What are frictional causes of keratoses?
Sharp teeth
Restorations
Dentures
Occlusion
242
What are thermal causes of keratoses?
Smoking
Hot food/drinks
243
What are chemical causes of keratoses?
Aspirin
Acid
Bleach
Chlorhexidine
244
What is the management of linea alba/frictional keratosis?
Identify cause
Correct cause and review 2-3 weeks later
If no improvement, consider referral or biopsy
245
What is the general management of white patches?
Thorough history and systems enquiry
Exclude red flags
Clinical photos
Correct obvious causes
If no improvement- refer
Consider need biopsy
246
Why do oral lesions appear to be red?
Inflammation
Mucosal atrophy
Increased vascularisation
Mucosal/submucosa bleeding
247
What are the differential diagnoses for red patches?
Viral infection
Candidal infection
Iatrogenic- mucositis secondary to chemo or radiotherapy
Lichen planus/lichenoid reactions
Granulomatous disease
Blistering diseases- vesticulobullous disorders
Allergy
Psoriasis
Geographic tongue
Leukaemia
Purpura
Trauma
Deficiency states
Erythroplakia
248
What is erythroplakia?
Atrophic lesion
Localised/focal
Well defined borders
Velvety/red texture
Speckled appearance (erythroleukoplakia)
Commonly affects soft palate/buccal mucosa/ FoM
Strong association with tobacco use
249
What % of erythoplakia showed invasive carcinoma?
51%
250
What % of erythroplakia showed carcinoma in situ?
40%
251
What % or erythroplakia showed moderate dysplasia?
9%
252
What is the % of malignant transformation rate of erythroplakia?
50%
253
What mutation is associated with erythroplakia?
p53
254
What is the management of erythroplakia?
Refer urgently to OMFS or OM
255
How does erythroleukoplakia present?
Speckled red/white patches
Heterogenous appearance
Highly suspicious for SCC or severe dysplasia
256
What is the management of red patches?
Through history and examination
Exclude red flags
Get photos
Correct obvious cause
Consider biopsy
257
What are exogenous causes of pigmented oral lesions?
Amalgam
Chlorhexidine
Tobacco
Heavy metals
258
What are endogenous causes of pigmented oral lesions?
Melanin
259
How doe amalgam tattoos present?
Amalgam fragments introduced into soft tissues
Blue/grey appearance
Consider radiograph or biopsy
260
What are examples of foreign bodies that can cause oral pigmentation?
Grit/dirt from road traffic accidents
Tattoos
261
What is peutz-jeghers syndrome?
Developmental hypermelanosis
Autosomal dominant disorder
Associated with STK11 (tumour suppressor gene mutation)
Resembles freckles; affects buccal mucosa and lips
Presents in infancy
262
What are the investigations for peutz-jeghers syndrome?
FBC
Endoscopy
STK11 gene
263
What is the treatment of peutz-jeghers syndrome?
Manage polyps
Regular MRI/CT
264
What is the effect of inflammation on melanocyte activity?
Stimulation causing increased melanin in areas of infection
265
What is the effect of Addisons disease on the oral cavity?
ACTH stimulates melanocytes leading to patchy hyperpigmentation
266
What medications are associated with oral pigmentation?
Antimalarials
Zidovudine- antiretroviral
Busulphan- chemotherapy
Gold
Minocycline- antibiotics
Heavy metal
267
What is a melanotic macule?
Single brown lesion compromised of melanin containing cells
Flat, non-raised, <1cm, no rapid change, painless
Common on vermillion border,
268
How should you manage a melanotic macule?
Consider excision biopsy to exclude melanoma
269
How does melanocytes naevi present?
Blue/black lesions
Focal proliferations of melanocytes
Appears during childhood
<1cm
Papular appearance
No rapid change
Clinically resemble melanoma
270
Where is melanoma in the oral cavity most common?
Palate or maxillary gingival
271
What factors are associated with suspected melanoma?
Asymmetry
Border Irregularity
Colour Irregularity
Diameter >6mm
Evolving (size, shape, colour, elevation)
272
What should you do with a suspected melanoma?
Refer urgently to OMFS
273
How common is melanoma?
1.2 cases per 10 millon per year
1-2% of oral malignancies
Average age 60
More common in more pigmented populations
274
What is the 5YS of melanoma?
25.5%
275
What is Kaposi's Sarcoma?
Vascular neoplasm associated with HHV8
Disorganised epithelial cell growth resulting in cleft containing erythrocytes
Redish-blue or brown foci
Presents on skin, oral mucosa and GI tract
276
What groups does Kaposi's Sarcoma most commonly affect?
Immunocompromised
Predilection for men who have sex with men
50% present in patients with untreated aids
Older Italian and eastern european jewish populations without imunodeficiency
277
What is the management of Kaposi's Sarcoma
Surgery
Radiotherapy
Chemotherapy
Immunotherapy
Manage underlying immunodeficiency (HAART)
278
What factors should be considered in the history of a patient with Kaposi's Sarcoma?
Onset of pigmentation
Appearance change
Symptoms
Other sites
PMH/Surgical History
Drug Hx
Tobacco/Betel use
Family history
Symptoms of systemic disease
279
What factors should be considered in the examination of a patient with Kaposi's Sarcoma?
Number of lesions
Diffuse or localised
Size/Borders/Colour
Variation in pigment
Inflammation/Ulceration
Lymphadenopathy
General examination
280
What blood tests should be carried out in secondary care for diffuse pigmented lesions?
FBC
U+E
LFT
Glucose
TFT
Cortisol/ACTH/Adrenal Antibodies
Ferritin
Bone Profile
HIV
Coeliac screen
280
What investigations can be carried out in secondary care for diffuse pigmented lesions?
Clinical photos
Lying/Standing BP - to exclude Addisons
Blood tests
Biopsy
Chest Xray- to exclude TB/Sarcoidosis (can cause adrenal insufficiency)
Endoscopy
281
What are the characteristics of viruses?
Small size
Simple chemical composition
No intracellular organelles
Genetic information kept in DNA or RNA
282
What are the stages of viral replication of herpes simplex?
1. Binding
2a/2b. Entry
3. Release and Nuclear Transport
4. Nuclear Entry
5. Gene Expression
6. DNA Replication
7. Packaging
8. Egress
283
What are the factors to consider in the history and examination in regard to laboratory diagnosis?
Ability to write referral letter or communicate via phone call
284
What are the features of a viral swab?
Flocked swab
Placed in molecular sample solution
After immersion the swab is removed
285
What tube is used for a blood sample?
EDTA (purple topped)
286
What can a blood sample be used for?
Serology or Molecular
287
What should be included on a virology request form?
Patient details and clinician details
Clinical details and provisional diagnosis
Date of onset
Patient DOB or CHI no
Specify tesy
288
What must specimens be transported in?
Approved containers
289
What are examples of common muculo papular/erythematous viral pathogens?
Enterovirus
HHV6
HHV7
Measles
Rubella
290
What type of specimen is taken for a maculo papular erythematous virus?
Mouth swap
291
What test is carried out for a maculo papular erythematous virus?
DNA/RNA detection
292
What are examples of common vesicular pathogens?
HSV1
HSV2
V2V
Enterovirus
293
What is the appropriate specimen for a vesicular pathogen?
Mouth swab
294
What is the appropriate test for a vesicular pathogen?
DNA/RNA detection
295
What are examples of common pathogens associated with ulcers?
HSV
Enterovirus
296
What is the appropriate specimen for ulcers?
Mouth swab
297
What is the appropriate test for ulcers?
DNA/RNA detection
298
What does serology detect?
Nucleic acid amplification or antibody levels
299
In regard to serology of a maculo papular/ erythematous lesion what are the common pathogens associated?
B19
CMV
EBV
300
What is the appropriate serology sample for maculo papular/ erythematous lesions?
EDTA blood
301
What is the appropriate serology test for maculo papular/ erythematous lesions?
DNA/RNA detection or serological markers
302
What Ig are CMV/EBV associated with?
IgM
303
What is VZV
Varicella Zoster Virus
304
What is HSV?
Herpes Simplex Virus
305
What are examples of oral viral infections?
Herpes simplex type 1
Herpes simplex type 2
Varicella zoster
Epstein barr
Cytomegalovirus
HHV-6
HHV-7
HHV-8 (Kaposi's sarcoma associated virus)
306
What are the common features of human herpes viruses?
Primary infection
Latency period
Recurrent infection
307
What are the clinical features of HHV 1 &2?
Gingivo stomatitis
Herpes labials
Keratoconjunctivitis
Herpetic whitlow
Bell's palsy
Genital herpes
308
What are the stages of herpes simplex pathogenesis?
Acute infection
Latency
Reactivation: Cold sores, viral shedding, epithelial cell death
309
310
What is the reservoir of HSV?
Saliva
311
What is the route of transmission of HSV?
Direct by close person to person contact
312
How can a lab diagnosis be made from vesicle/ulcer fluid?
Swab and molecular sample for PCR
313
What is the prevention of HSV?
Chemoprophylaxis: Aciclovir to prevent recurrent infection in difficult cases (200mg x5 daily)
314
What is the treatment of HSV?
Topical therapy with Aciclovir (5% cream)
IV therapy for severe and immunocompromised
315
What are the clinical features of varicella zoster virus?
Incubation period of 10-21 days
316
What are the signs and symptoms of shingles?
Vesicles appear in dermatome, representing cranial or spinal ganglia where the virus has been dormant
The affected area may be intensely painful with associated paraesthesia
316
What are the complications of varicella zoster virus? (chicken pox)
Secondary bacterial infections
Pneumonia
Problems in pregnancy; Congenital, perinatal/neonatal
317
What are the complications of varicella zoster virus? (shingles)
Post herpetic neuralgia
Secondary bacterial infection
Ophthalmic zoster
Ramsay Hunt Syndrome
318
What is the pathogenesis of varicella zoster?
Primary infection- varicella zoster virus (chicken pox)
Latency- sensory ganglion (trigemina)
Recurrent Infection: Reactivation of latent virus from sensory ganglion
319
What is the epidemiology of varicella zoster?
Very common >90%
320
What is the mode of transmission of varicella zoster?
Contact with varicella or zoster
321
What is the varicella form?
Chicken pox
322
What are the features of varicella?
Highly infections especially the respiratory secretions, the vesicles are also infectious
48 hours before symptoms
323
What is zoster?
Shingles
324
How is shingles developed?
From the latent virus in the sensory ganglion
325
What is the rate of transmission of zoster from vesicle fluid?
Low
326
What is the route of transmission of VZV?
Direct contact
Droplet or airborne spread
327
What is the occurrence of varicella?
Highest in children
328
What is the occurrence of zoster?
Highest in elderly and immunocompromised
329
How many cases of zoster is there per year in Scotland?
7000
330
How many people develop post herpetic neuralgia from zoster in Scotland per year?
700-1400
331
How many people are admitted to hospital from complications with post herpetic neuralgia in Scotland per year?
600
332
What sample should be taken for zoster?
Vesicle/ulcer fluid for swab and molecular sample for PCR
333
Who is offered the chicken pox vaccine?
People in close contact to someone who is particularly vulnerable to chicken pox or its complications
334
What is the treatment of shingles?
Anti viral therapy: Aciclovir 800mg oral x5 daily for 7 days
335
What is the prevention of zoster?
Vaccine: Zostavax
336
What type of vaccine is Zostavax?
Live attenuated virus
337
Who received zostavax?
All people aged over 70
338
What is the efficacy of Zostavax?
62%
339
What was the % decrease of post herpetic neuralgia following the Zostavax?
70-88%
340
What are the symptoms of hand, food and mouth disease?
Fever
Runny nose
Sneezing
Coughing
Skin rash
Mouth blisters
Body and muscle aches
341
What is the pathogenesis of hand, foot and mouth disease?
Enterovirus
A large group of virus
Transmitted though nose and throat secretions or fluid from blisters scabs or faeces
342
What is the dentally relevant non-polio enterovirus?
Coxsackie virus
343
When is hand, foot and mouth most infectious?
1st week of disease
344
What is the epidemiology of hand, foot and mouth disease?
Common in children under 5
Very contagious
345
What type of sample can be taken for suspected hand, foot and mouth disease?
Oral swab
346
What can be done in the prevention of hand, foot and mouth?
Hand hygiene
347
What can be done in the treatment of hand, foot and mouth?
Relieve symptoms and prevent dehydration
348
What is the animal equivalent of hand, foot and mouth?
Foot and mouth disease
349
What are the signs and symptoms 7-14 days after an exposure to measles?
High fever
Cough
Runny nose
Conjunctivitis
350
What are Koplik spots?
Tiny white spots inside the mouth
Occur 16-7 days after exposure to measles
351
What are the signs and symptoms 3-5 days after Koplik spots have developed?
A rash begins on the face and spreads downwards
352
What are examples of complications of measles?
Pneumonia
Brain swelling
Diarrhea
Death
Hearing loss
353
What is the R number of measles?
18
354
How long can measles virus live on surfaces?
2 hours
355
What is the laboratory diagnosis of measles?
PCR from mouth swab
356
What is the incubation period of mumps?
12-24 days
357
What are the signs and symptoms of mumps?
Headache and fever
Swelling of the parotid glands
358
What type of virus is mumps?
Paramyxovirus family
RNA virus
359
How is mumps transmitted?
Direct contact with saliva/fomites or aerosol
360
What sample is taken for lab diagnosis of mumps in Scotland?
Oral swab for RNA detection
361
What sample is taken for lab diagnosis of mumps in England?
Oral fluid samples
Oral fluid IgM antibody tests
PCR
362
What is the epidemiology of mumps?
Notable outbreaks in student populations linked to MMR vaccine distribution
363
What is the treatment of mumps?
Symptom relief
364
What is the prevention of mumps?
Routine vaccination
365
When do symptoms begin for monkeypox?
5-21 days after exposure
366
What are the clinical features of monkeypox?
Rash 1-5 days post fever
Blistering rash or skin lesions on face and genital area
Most common in males- identifying as gay/bisexual/have sex with other men
Clinical diagnosis is difficult
367
What type of virus is monkey pox?
Enveloped DNA virus
Zoonotic disease
368
How is monkeypox transmitted?
Close contact with an infected person or animal or contaminated material
369
How many cases of monkey pox has there been worldwide?
71,237
370
What is the lab diagnosis method for monkey pox?
PCR for viral DNA from swabs
371
What is the prevention of monkeypox?
Vaccination: modified vaccinia Ankara (MVA)
372
What is aciclovir?
Antiviral medication
An acrylic purine nucleoside
372
What type of vaccine is modified vaccinia Ankara?
Live Attenuated
373
How does aciclovir work?
Inhibits DNA polymerase in viruses
374
Discuss the steps in the mechanism of action of aciclovir:
Viral enzymes add a phosphate group to acyclovir
Human enzymes add two more phosphate groups producing acyclovir triphosphate
During viral DNA replication, acyclovir is added to the growing strand rather than GTP. This halts further elongation of the DNA molecule and stops viral replication
375
What is the viral enzyme (aciclovir)?
Thymine kinase
376
What are the uses of aciclovir?
Management of herpes simplex and zoster infections
377
How does resistance to aciclovir occur?
Mutations in viral thymine kinase
378
What is the definition of a vesicle?
<5mm visible accumulation of fluid within or beneath epithelium
379
What is a bullae?
>5mm visible accumulation of fluid within or beneath epithelium
380
What are some examples of vesiculobullous conditions?
Mucous membrane pemphigoid
Pemphigus vulgaris
Erythema multiforme
Stevens-Johnson syndrome/toxic epidermal necrolysis
381
What are the oral/lip features of vesiculobullous conditions?
Vesicles
Bullae
Ulcers
382
What are the oral/lip features of vesiculobullous conditions?
Vesicles
Bullae
Ulcers
383
What is the mucosal involvement associated with vesiculobullous conditions?
Oesophageal
Ocular
Nasal
Anogenital
384
What are the features of oral mucosa?
Epithelium (keratinocytes): stratified squamous
Basement membrane: Non-cellar interface
Lamina propria: collagen, fibroblasts, nerves, blood vessels
Desmosomes: joins kertainocytes
Hemi-desmosomes: joins basal keratinocytes to basement membrane
385
What are the features mucous membrane pemphigoid?
Autoimmune process
50-60 years
1M:2F
386
What are the clinical features of mucous membrane pemphigoid?
Oral vesicles/blisters —> ulcers
Desquamative gingivitis
Ocular lesions —> conjunctival scarring
Anogenital lesions
Skin lesions (scalp)
Nasal mucosa
387
What are the clinical features of mucous membrane pemphigoid?
Oral vesicles/blisters —> ulcers
Desquamative gingivitis
Ocular lesions —> conjunctival scarring
Anogenital lesions
Skin lesions (scalp)
Nasal mucosa
388
What is the aetiology of mucous membrane pemphigoid?
Unknown
Likely genetic predisposition
Autoimmune
389
What is the Pathogenesis of mucous membrane pemphigoid?
Antibody (IgG) targeting the basement membrane zone (hemidesmosomes)
Complement activation
Subepithelial splitting- vesicles, blisters, ulcers
390
How is mucous membrane pemphigoid diagnosed?
Biopsy:
H&E staining
Direct immunofluorescence microscopy (DIF)- from perilesional tissue
Indirect immunofluorence
391
How is mucous membrane pemphigoid diagnosed?
Biopsy:
H&E staining
Direct immunofluorescence microscopy (DIF)- from perilesional tissue
Indirect immunofluorence
392
What is direct immunofluorescence?
Tissue (biopsy) is put onto slide and processed
Antibody (bound to fluorophore) specific to IgG, IgA, C3 are applied to the tissue
Examined with UV microscope
Fluorescence at area of binding
393
What is indirect immunofluorescence?
Blood sample taken (containing the primary disease antibody)
Incubated with normal mucosa (monkey oesophagus)
Addition of (secondary) antibody + flurrophore
Tissue examined
If antibodies present in serum, will show in tissue
394
What is the management of Mucous Membrane Pemphigoid?
MDT Approach: Oral medicine, opthamology, gynaecology, dermatogy
Low risk- oral disease only
High risk- multi site
395
What is the management of mucous membrane pemphigoid?
Patient education
Oral disease severity score
Symptomatic relief (benzydamine mouthwash)
Oral hygiene
Topical corticosteroids:
Intralesional steroid injection:
Systemic treatment:
396
What are the topical corticosteroid used for mucosal membrane pemphigoid?
Mouthwash (betamethasone)
Custom made tray (clobetasol)
397
What are intralesional steroid injection?
Triamcinolone
398
What are examples of systemic treatments for mucosal membrane pemphigoid?
Prednisone (pulsed)
Dapsone
Doxycycline
Azathioprine
Mycophenolate mofetil
Methotrexate
Rituximab
IV immunoglobulins
399
What is pemphigus vulgaris?
Autoimmune condition with a female preponderance
400
What are the clinical features of pemphigus vulgaris?
Oral bullae (quickly rupture to leave erosions/ulcers)
Desquamative gingivitis
Ocular involvement
Aerodigestive tract
Anogenital blistering
Skin
Pain
Potentially lethal
Systemically unwell: impaired oral intake, sepsis
401
What are the clinical features of pemphigus vulgaris?
Oral bullae (quickly rupture to leave erosions/ulcers)
Desquamative gingivitis
Ocular involvement
Aerodigestive tract
Anogenital blistering
Skin
Pain
Potentially lethal
Systemically unwell: impaired oral intake, sepsis
402
What is the aetiology of pemphigus vulgaris?
Autoimmune overlap
403
What is the aetiology of pemphigus vulgaris?
Autoimmune overlap
404
What is the Pathogenesis of pemphigus vulgaris?
Antibodies (mainly IgG) directed against desmosomes
Loss of cell-cell contact in epithelium- ‘acantholysis’
Intra-epithelial split forms
Flaccid blisters (cf MMP)
405
What is the Pathogenesis of pemphigus vulgaris?
Antibodies (mainly IgG) directed against desmosomes
Loss of cell-cell contact in epithelium- ‘acantholysis’
Intra-epithelial split forms
Flaccid blisters (cf MMP)
406
How is pemphigus vulgaris diagnosed?
Nikolsky’s sign
Biopsy; H&E staining (from affected tissue), direct immunofluorescence microscopy (DIF)- from perilesional tissue
Indirect immunofluorescence- blood sample (more sensitive in PV than in MMP)
407
How is pemphigus vulgaris diagnosed?
Nikolsky’s sign
Biopsy; H&E staining (from affected tissue), direct immunofluorescence microscopy (DIF)- from perilesional tissue
Indirect immunofluorescence- blood sample (more sensitive in PV than in MMP)
408
What is nikolsky’s sign?
Rubbing the mucosa induces a bulla
409
What is nikolsky’s sign?
Rubbing the mucosa induces a bulla
410
How does pemphigus vulgaris present in a H&E staining?
Intra-epithelial acantholysis
411
How does pemphigus vulgaris present on a direct immunofluorescence (DIF)?
Intercellular deposition of IgG and C3- chicken wire appearance
412
How does pemphigus vulgaris present on a direct immunofluorescence (DIF)?
Intercellular deposition of IgG and C3- chicken wire appearance
413
How does pemphigus vulgaris present on a indirect immunofluorescence (DIF)?
Titre of autoantibody correlates with disease severity
414
How does pemphigus vulgaris present on a indirect immunofluorescence (DIF)?
Titre of autoantibody correlates with disease severity
415
What is the MDT management of pemphigus vulgaris?
IV fluid resuscitation
Feeding
Management of secondary infection
Analgesia
416
What is the MDT management of pemphigus vulgaris?
IV fluid resuscitation
Feeding
Management of secondary infection
Analgesia
417
What are the two main phases of the management of pemphigus vulgaris?
1. Induction of remission
2. Maintainance
418
What does the induction of remission stage of pemphigus vulgaris treatment involve?
Prednisolone (+/- bone/gastric protection)
Commence second agent (Aza, MMF, rituximab)
419
What does the maintenance phase of pemphigus vulgaris treatment involve?
Gradular withdrawal of oral steroids (aim <10mg prednisolone)
Second agent
Regular monitoring (ODSS)
Topical steroids
Benzydamine
Excellent OH
420
What is paraneoplastic pemphigus?
Rare variation of PV
Associated with an underlying malignancy (usually haematological malignancy)
Presents with severe mucosal and skin involvement
High mortality
421
What is erythema multiforme?
Acute onset
Hypersensitivity reaction (often triggered)
25% recurrence
422
What age group is affected by erythema multiforme?
10-40 years
423
What age group is affected by erythema multiforme?
10-40 years
424
What are the clinical features of erythema multiforme?
Flu-like prodrome (1-2 weeks)
Skin- classical target lesion, itchy
Lip blisters, ulceration and crusting
Oral ulcers (particularly anteriorly)
Other mucosal affected- eyes, genitals
425
What are the clinical features of erythema multiforme?
Flu-like prodrome (1-2 weeks)
Skin- classical target lesion, itchy
Lip blisters, ulceration and crusting
Oral ulcers (particularly anteriorly)
Other mucosal affected- eyes, genitals
426
What is the difference between minor and major erythema multiforme?
Minor- oral +/- skin targets
Major- oral, skin and other mucosa site
427
What is the aetiology of erythema multiforme?
Hypersensitivity
Infective
Drugs
Following BCGs or Hep B immunisations
428
What are the infective aetiological factors associated with erythema multiform?
Herpes simplex virus (HSV-1) in 15-20%
429
What are the drug related factors associated with erythema multiform?
Allopurinol
Carbamazepine
NSAIDs
Phenytoin
430
What is the Pathogenesis of erythema multiform?
Release of cytokines from CD4 cells
Amplified immune response
CD8 T cells attack keratinocytes
Apoptosis and necrosis of keratinocytes
431
How is erythema multiform diagnosed?
Clinical history - triggering agent
Biopsy of perilesional tissue- histology: lymphocytic infiltrate, keratinocytes necrosis, intra and sub epithelial splitting
Immunofluorescence
HSV serology/throat swabs for mycoplasma pneumoniae
432
How is erythema multiform managed?
MDT approach: feeding/fluids
Stop any obvious precipitating medications
Topical steroids for oral lesions (minor EM), systemic steroids for more serious disease
Adjunctive oral care (hygiene, CHX, comfort measures)
Antihistamines for skin itch
433
How is recurrent erythema multiform managed?
Consideration of immunosuppression (Aza, MMF)- risk/benefit
Prophylactic aciclovir (due to HSV implication)
434
What is Steven-Johnson Syndrome (SJS)/ Toxic Epideral necrolysis (TEN)?
Rare
Very severe- critical care admission
Spectrum
Wide spread blistering of skin and oral, pharyngeal genital, nasal and conjunctival involvement
435
What is the aetiology of SJS/TEN?
Hypersensitivity to medications: allopurinol, carbamazepine, NSAIDs, phenytoin, penicillins
Genetic predisposition
Association with HIV
436
What is the Pathogenesis of SJS/TEN?
Antigens (medication) presented to T lymphocytes
Dysregulated immune reaction
CD8 cells, macrophages and neutrophils into epithelium
Release of granulysin- pore-forming peptide
Apoptosis, necrosis of keratinocytes
Breach of skin/mucosa (skin failure)
437
How is SJS/TEN diagnosed?
Clinical history and exam
Skin biopsy- epidermal necrosis, detachment from dermis
438
How is SJS/TEN diagnosed?
Clinical history and exam
Skin biopsy- epidermal necrosis, detachment from dermis
439
What is the TBSA and mortality rate of SJS?
<10% TBSA
1-5% mortality rate
440
What is the TBSA of SJS/TEN overlap?
10-30% TBSA
441
What is the TBSA and mortality rate of TEN?
>30% TBSA
30% mortality rate
442
What is the TBSA and mortality rate of TEN?
>30% TBSA
30% mortality rate
443
How is SJS/TEN managed?
Urgent assessment in specialist centre- burns unit, ITU
A-E approach
Stop causative agent (medication)
MDT approach
444
How is SJS/TEN managed?
Urgent assessment in specialist centre- burns unit, ITU
A-E approach
Stop causative agent (medication)
MDT approach
445
What is the A-E approach in SJS/TEN?
A Airway involvement- intubation
B Ventilatory support
C Guided fluid resuscitation
D Sedation/pain management
E Temperature management, secondary infection, NG feeding
446
What is the A-E approach in SJS/TEN?
A Airway involvement- intubation
B Ventilatory support
C Guided fluid resuscitation
D Sedation/pain management
E Temperature management, secondary infection, NG feeding
447
What is the MDT approach to SJS/TEN?
Dermatology, ophthalmology, ENT, burns team
CHX, oral lubricants, topical steroid
Skin/wound management
Eye care
448
What are examples of fungal oral infectious disease?
Candida
449
What are examples of viral infectious diseases?
Herpes simplex
Varicella zoster
Human immunodeficiency virus
Hepatitis C
Coxsackie virus
450
What are examples of bacterial oral infectious diseases?
Syphilis
Gonorrhoea
Chlamydia
Tuberculosis
451
What is candidosis?
Infection of mucosa caused by candida species
452
What % of normal population are carriers of Candida albicans?
70%
453
What are local defences to candida?
Oral mucosa: physical barrier, innate immunity (lysozyme, T cells, phagocytes)
Oral microbiome: competition and inhibition
Saliva: mechanical cleansing, antimicrobial peptides (mucins, defensins, histatins), IgA antibodies
454
What are systemic defences to candida?
Immune system; adaptive immunity
455
What are local risk factors to oral candidosis?
Xerostomia
Poor OH
Dental appliances
Mouth piercings
Smoking
Irradiation to mouth/salivary glands
Inhaled/topical corticosteroids
456
What are the systemic risk factors to candidosis?
Extremes of age
Malnutrition
Diabetes
HIV/AIDS
Haemantinic deficiency
Broad spectrum antibodies
Chemotherapy
Haematological malignancy
457
How are candidal infections managed?
Investigate and manage predisposing factors
Oral hygiene
Topical anti fungal a
458
What questions should you investigate when managing a patient with candida?
Does this person have underlying systemic disease or deficiency ?
Do they smoke?
Do they have a dry mouth?
Do they use a steroid inhaler?
Consider dentist hygiene
459
What topical anti fungals are used for candida?
Miconazole gel
Nystatin oral mouthwash
460
When should miconazole be avoided?
warfarin/ statins
461
What systemic antifungals can be given for candida infections?
Fluconazole
462
What systemic antifungals can be given for candida infections?
Fluconazold
463
What is the prescription for nystatin in candida patients.
20mg/g
Send 80g tube
Apply a pea sized amount after food 4 times daily
464
What is the interaction of warfarin and miconazole?
Increases anticoagulant effect (increases INR)
465
What is the interaction between miconazole and statins?
Risk of rhabdomyolysis and myopathy with some statins
466
What is the prescription for nystatin oral suspension for candida patients?
100,000 units/ ml
Send 30ml
Label 1ml after food 4 times daily for 7 days
Continue use for 48 hours after lesions have healed
467
What is the prescription for fluconazole in candida patients?
50mg
Send 7 capsules
Label 1 capsule daily
468
When should you not prescribe fluconazole?
Warfarin and statins
469
When should you not prescribe fluconazole?
Warfarin and statins
470
What is the interaction of fluconazole and warfarin?
Increased anticoagulant effect
471
What is the interaction between fluconazole and statins?
Risk if rhabdomyolysis and myopathy
472
What are the types of candidal infections?
Acute psuedomembranous candidosis
Chronic hyperplastic candidosis
Denture related stomatitis
Acute erythematous glossitis
Angular cheilitis
473
What is acute pseudonenbranous candidosis also known as?
Thrush
474
What age group is most commonly affected by acute pseudomembranous candidosis?
Neonates
475
How does acute psuedomembranous candidosis present?
White slough on mucosa surface (easily wiped off)
Underlying erythenatous base
476
How is acute psuedomembranous candidosis diagnosed?
Clinically
Microbiology investigations: oral rinse, oral swab
477
How is acute psuedomembranous candidosis managed?
Predisposing factors investigated and managed
Oral hygiene
Topical: miconazole oral gel , nystatin oral mouth wash
Systemic (if topical ineffective or severe disease)- fluconazole capsules
478
What is chronic hyperplastic candidosis also known as?
Candidal leukoplakia
479
What is the risk of chronic hyperplastic candidosis?
Potentially malignant disorder
480
How does chronic hyperplastic candidosis present?
Usually on buccal mucosa (at labial commissure)
Often bilateral
Can occur less commonly on tongue
481
How is chronic hyperplastic candida managed?
Incisional biopsy (with periodic acid schiff stain)
482
Why should you prescribe fluconazole before biopsy of suspected chronic hyperplastic candidosis?
To allow pathologist to see potential dysplasia more clearly
Fungal related inflammation can give fake positive for dysplasia
483
How is chronic hyperplastic candidosis managed?
Predisposing factors
Systemic antifungals
Stop smoking
Careful clinical follow up
Manage of dysplasia as required
484
What is denture related stomatitis?
Candidal infection of mucosa beneath a dental appliance
485
What group is denture related stomatitis most associated with?
Care facilities: elderly, dry mouth, high sucrose diet, lack of oral hygiene
486
What type of denture is most associated with denture related stomatitis?
Upper complete
487
What % of denture related stomatitis is candida?
90%
488
What is involved in a mixed infection of denture related stomatitis?
Candida
Staphylococcus
Streptococcus
489
What features of dentures lead to a good habitat for candidal adherence?
Acrylic resin
Soft liners
490
How is denture related stomatitis diagnoses?
Clinical diagnosis
491
What is newtons class 1?
Localised inflammation (pinpoint)
492
What is newtons class 1?
Localised inflammation (pinpoint)
493
What is newtons class 2?
Generalised erythema covering the denture bearing area
494
What is newtons class 3?
Granular type
495
What is the management of denture related stomatitis?
Predisposing factors
Denture hygiene
Oral hygiene (brushing palate)
Antifungals (last resort); miconazole to surface of denture
496
What denture hygiene advice should be given to a denture related stomatitis patient?
Remove denture at night
Gently daily brushing
Chlorhexidine immersion
Dilute hypochlorite immersion
Microwave disinfection
Alkaline peroxide
Remake if required
497
What is acute erythematous candidiasis also known as?
Atrophic candidiasis
498
How does acute erythematous candidiasis present?
Burning
Usually affects palate
499
What are examples of predisposing factors to acute erythematous candidiosis?
Recent broad spectrum antibiotics
Corticosteroids
Diabetes
HIV
Nutritional factors
500
How is acute erythematous candidiasis diagnosed?
Clinical
Oral rinse/oral swab
501
How is acute erythematous candidiasis managed?
Medical referral (?)
Topical antifungal
Systemic anti fungal
502
Where does median rhomboid glossitis?
Posterior aspect/midline of tongue dorsum
503
How does median rhomboid glossitis present?
Depapillitation in irregular shape
May have a kissing lesion on the palate
504
What is median rhomboid glossitis associated with?
Steroid inhalers
Smokers
505
How is median rhomboid glossitis diagnosed?
Clinical
506
How is median rhomboid glossitis managed?
Predisposing factors
Oral/denture hygiene
Topical antifungal
Systemic antifungal
507
What is angual cheilitis?
Infection of mucocutaneous region around corners of mouth, often associated with dermatitis
508
What is involved in a mixed annual cheilitis infection?
Candida
Staphylococcus
Streptococcus
509
How does angular cheilitis present?
Soreness
Erythema
Fissuring
Crusting
Bleeding
510
What mechanical factors play a role in angular cheilitis?
Ageing
Edentulous
Dentures lacking in vertical height (encourages saliva pooling)
511
How is angular cheilitis diagnosed?
Clinical diagnosis
Swab for microbiology
512
How is angular cheilitis managed?
Predisposing factors (new dentures, underlying disease/deficiency?)
Denture hygiene and oral hygiene
Topical antifungal - micoazole cream
Topical antibacterial- sodium fusidate ointment (when clearly bacterial nature- non-denture wearer)
513
What is the prescription for sodium fusidate?
Sodium fusidate ointment 2%
Send 15g tube
Label apply to angles of mouth four times daily
514
Why is sodium fusidate to not be used for longer than 10 days?
To avoid the development of resistance
515
What is the treatment of angular cheilitis if there is significant associated dermatitis?
Combined miconazole and hydrocortisone cream/ointment
cream for wet surface
ointment for dry surface
516
What is the prescription for miconazole and hydrocortisone cream?
Miconazole (2%) and Hydrocortisone (1%)
Send 30g tube
Label apply to angles of the mouth twice daily
maximum of 7 days
517
What are human herpes viruses?
Family of DNA viruses
Transmitted in saliva, respiratory secretions and direct contact
518
When do human herpes viruses reactivate?
When immunity drops
519
What is the difference between HSV 1 and HSV 2?
1- oral
2- anogenital
520
How does the primary HSV1/2 infection present?
Lesions in mouth, oropharynx and ano-genital lesions
521
When does primary infection of HSV1 and 2 usually occur?
2-4 years
522
How is HSV1 and 2 transmitted?
Close contact (saliva)
523
What are the symptoms of primary infection of HSV 1 and 2?
Fever
Malaise
Red, fiery oedematous gingival
Vesicles --> ulcers
524
How is primary herpetic gingivostomatitis diagnosed?
Clinical (and history)
Viral swab for PCR
525
How is primary herpetic gingivastomatitis managed?
Largely supportive: fluids, paracetamol, soft diet, chlorhexidine mw, difflam mw
Pregnant women and neonates- urgent specialist care
526
What % of the population has recurrent herpes simplex virus?
15%
527
What is another name for cold sores?
Herpes labialis
528
What can reactivate herpes simplex virus?
Sunlight (UV radiation)
Unwell (fever)
Tissue injury
Stress
Immunosuppression
Hormonal (menstrual cycle)
529
How does recurrent herpes simplex virus present?
Prodromal period- pain, burning, tingling, itching (up to 48 hrs before)
Herpes labialis and intra-oral herpes
Crops of ulcers- scab within 72 hours, resolve by 10 days
530
How is recurrent herpes simplex virus diagnosed?
Clinical
531
How is recurrent herpes simplex virus managed?
Avoidance of triggers
Antivirals in prodrome period;
5% Aciclovir cream every 2 hours herpes labials
Aciclovir 200mg tablets 5 times a day for 5 day intra-oral herpes
Immunocompromised- specialist referral
532
What antiviral should be prescribed for herpes labialis?
Aciclovir 5% every 2 hours
533
What antiviral should be prescribed for intra oral herpes?
Aciclovir 200mg
534
What are the complications of recurrent herpes simplex virus?
Disseminated herpes infection (immunocompromised)
Bell's palsy
Erythema multiforme
Herpetic whitlow (fingers)
Eye disease (herpetic keratoconjunctivitis)
535
Where does latent varicella zoster virus lie?
In the Doral root ganglion
536
How does varicella zoster spread?
Respiratory droplets or lesion
537
How does varicella zoster present?
Fever
Malaise
Truncal rash- itchy, papules, vesicles, scabs
Oral ulcers
538
How is varicella zoster managed?
Supportive
Immunocompromised, pregnant and neonates- specialist care
539
How does zoster present?
Rash in one dermatome --> scabs
Pain before, during and after lesions
Vesicles and ulcers intra-orally
540
How is zoster diagnosed?
Clinically
541
How is zoster managed?
Aciclovir 800mg tablets (within 72 hours od onset)
Refere to GP
Immunocompromised- to specialist
542
What is the prescription for acyclovir for zoster?
Aciclovir 800mg
Send 35 tablets
Label 1 tablet 5 times daily
543
What are the complications of zoster virus?
Post herpetic neuralgia
Ramsay hunt syndrome
544
What is post herpetic neuralgia?
Burning pain
Persists 6 months after mucocutaneous healing
545
What medication is used to treat post herpetic neuralgia?
Gabapentin
Amitriptyline
Nortriptyline
Carbamazepine
546
What is Ramsay Hunt syndrome?
Reactivation within geniculate ganglion (CN7)
547
How does Ramsay Hunt syndrome present?
Facial nerve palsy
Vesicular rash around ear and oral vesicles
548
What % of the population have Epstein Barr Virus?
95%
549
How is Epstein Barr virus transmitted?
Saliva
550
What is glandular fever also known as?
Infectious mononucleosis
551
Where does Epstein Barr virus lie during latency period?
Lymphoid tissue
552
What may Epstein Barr virus reactivate as?
Oral hairy leukoplakia
Burkitts lymphoma
Nasopharyngeal cancer
553
What conditions is hairy leukoplakia associated with?
HIV positive patients (when CD4 count drops)
Seen in chemotherapy, leukoplakia
554
Where is oral hairy leukoplakia found?
Lateral aspect of tongue
555
How is oral hairy leukoplakia diagnosed?
Incisional biopsy
Immunohistochemistry for EBV
556
Where is human herpes virus 8 found?
Endothelial cells of blood and lymphatic vessels
557
How is human herpes virus 8 diagnosed?
Incisional biopsy
558
How is human herpes virus 8 managed?
Underlying immunosuppression- HAART in HIV
Excision
Cryotherapy
Intralesional vinblastine
Chemotherapy
559
What is HAART?
Highly active antiretroviral therapy
560
What is HIV?
Blood borne RNA virus
561
How is HIV transmitted?
Sexual transmission
Needle stick injuries
Splashes
Vertical transmission
562
What does HIV do?
Enters and destroys CD4 T helper cells
563
What does AIDS stand for?
Acquired Immunodeficiency Syndrome (AIDS)
564
What is the treatment of HIV?
ART
PrEP
PEP
565
How many people in UK have HIV?
105,300
566
What % of HIV patients in UK are virally suppressed?
97%
567
What is the testing for HIV?
Blood test- look for antibodies and p24 antigen
568
What is ART?
Anti retroviral therapy
569
What does ART do?
Halts HIV replication
Causes a normal CD4 count and undetectable viral load
Can cause oral hyperpigmentation
570
What are AIDs defining illnesses?
Kaposi Sarcoma
Pneumocystis jirovecci pneumonia (PCP)
Cytomegalovirus infection
Candidiasis
Lymphomas
Tuberculosis
571
What are oral AIDS defining illnesses?
Oral candidosis
Acute necrotising ulcerative gingivitis
Kaposis sarcoma
Oral hairy leukoplakia
Non-hodgkins lymphoma
Aphthous like ulcers
572
What is Hepatitis C?
RNA virus that infects liver leading to chronic infection
573
How is hepatitis C spread?
Blood and bodily fluids
574
What are the complications of hepatitis C?
Liver cirrhosis
Hepatocellular carcinoma
575
What is the cure for hepatitis C?
Antiviral medication for 8-12 weeks
576
What condition is hepatitis C associated with?
Oral lichen planus
577
What is coxsackie virus?
Family of RNA virus
578
How does coxsackie virus spread?
Faecal-oral route
Saliva
579
How does coxsackie virus present?
hand, foot and mouth disease
Herpangina
580
Who is affected by coxsackie virus?
Young children
581
What are the systemic symptoms of coxsackie virus?
Fever
Reduced appetite
Malaise
582
How does coxsackie virus present on hands, feet and mouth?
Vesicles/blisters
(labial, buccal and tongue mucosa)
583
How does herpangina present?
Numerous vesicles on the soft palate, uvula and sauces
584
How is coxsackie virus diagnosed?
Clinical
585
How is coxsackie virus managed?
Supportive
Fluids
Paracetamol, ibuprofen
Soft diet
Chlorhexidine to aid OH
Difflam mouthwash
586
What are examples of bacterial infections?
Periapical infection
Periodontal infection
Pericoronal infection
Bacterial sialadenitis
587
What are the risk factors for STIs?
Previous STI
Under 25 years
New sexual partner
More than one sexual partner in the last year
No condom use
Paying for sex
Socioeconomic deprivation
Chemsex
588
What is syphilis?
Sexually transmitted disease
589
What bacteria is syphilis associated with?
Spirochete treponema palladium
590
What % of GBMSM account for new syphilis diagnoses?
76%
591
How does primary syphilis present?
Chancre at site of inoculation
Painless ulcer
Usually genital but can be oral
Self limiting- heals by 8 weeks
Associated lymphadenopathy (80%)
Untreated infection spreads lymphovascular
592
How does secondary syphilis present?
4-6 weeks after initial infection
Non-specific symptoms- lethargy, malaise, fever, musculoskeletal pain, rash
Mucosal white patches
Snail track ulcers
Condloma lata
593
How does tertiary syphilis present?
Progression from untreated infection
Presents 1-30 years after innoculation
Gummatous lesions (granulomatous infection)
Neurosyphilis (dementia, cranial nerve palsy)
Cardiovascular syphilis (aortic aneurysms)
594
How is syphilis diagnosed?
Incisional biopsy- for microscopy and immunohistochemistry
Blood test- IgG and IgM antibodies to Treponema palladium
595
How is syphilis managed?
By sexual health specialist (GUM clinic)
STAT doses of IM benzylpenicilin
Screening for other STIs
Contact tracing
596
What bacteria is gonorrhoea associated with?
Neisseria gonorrhoea
597
What bacteria is chlamydia associated with?
Chlamydia trachomatis
598
Where does gonorrhoea and chlamydia affect?
Urethra
Endocervix
Rectum
PharynxWh
599
What are the symptoms of gonorrhoea and chlamydiua?
Male- urethral discharge, dysuria
Female- altered vaginal discharge, dyuria
600
What is the oral presentation of gonorrhoea and chlamydia?
Pharyngitis
601
How is gonorrhoea and chlamydia diagnosed?
Clinical - oral
Specialist- vulvovaginal or urethral swabs (NAAT), swab for microscopy culture and sensitivity
602
How is gonorrhoea and chlamydia managed?
By sexual health specialist (GUM clinic)
Gonorrhoea STAT dose of IM ceftriaxone/ Chlamydia 7 days oral doxycycline
Screening for other STIs
Contact tracing
603
What bacteria is associated with tuberculosis?
Mycobacterium tuberculosis
604
How many deaths globally due to tuberculosis?
1.5m
605
How is tuberculosis transmitted?
Respitatory secretions
606
How does tuberculosis present?
Fever, weight loss, night sweats
Cough, haemoptysis
607
What are the risk factors of tuberculosis?
Close contact with tb patient
Born in high prevalence regions (India, Pakistan, Somalia, Eritrea, Romania)
HIV
Diabetes
Leukaemia
Alcohol excess
Socioeconomic deprivation
Homelessness
608
What are the oral manifestations of tuberculosis?
Ulceration
Lip swelling
609
How is tuberculosis diagnosed?
Incisional biopsy- H+E, Ziehl-Neelsen staining
610
611
What is the prevalence of Recurrent Apthous Stomatitis?
5-60% depending on population
612
What is the aetiopathogenesis of recurrent apthous stomatitis?
Idiopathic
Strong associations: FH, Nonsmoker or smoking cessation, trauma, haemantinic deficiencies, age >30 years
Weak associations: female, higher SES, high stress, food intolerance, hormonal imbalance, SLS containing toothpaste and drugs
613
What is the aetiopathogenesis of recurrent apthous stomatitis?
Idiopathic
Strong associations: FH, Nonsmoker or smoking cessation, trauma, haemantinic deficiencies, age >30 years
614
What knowledge is developing in regard to recurrent apthous stomatitis?
Multiple genetically identified HLAs identified
Cytokine polymorphism recently implicated as a predisposing factor
615
What are examples of the immunological response in RAS?
Reactivation and hyper-reactivity of neutrophils
Increased number of NK cells
High level of the complement system ingredients
Increased number of B lymphocytes
Decreased activity of regulatory Treg CD4+ CD25+ lymphocytes
Decreased number of CD4+ lymphocytes- disrupted CD4+/CD8+ ratio
Increased number of TyAlpha cells
Decreased expression of HSP
Limited expression of anti-inflammatory Th2-type cytokines and TCF-B
Preponderance of pro inflammatory Th1 type cytokines (Il-2, Il-12, IFN-y, TNF-Alpha)
616
How is recurrent apthous stomatitis diagnosed?
Clinical diagnosis (of exclusion)
No single diagnostic test- ulcer history, medical history, medications, systems enquiry
617
What are the factors of an ulcer history?
Onset
Number
Duration
Frequency
Pattern
Location
Size
Pain
Prodrome
Associated symptoms
Triggers
Relievers
Previous treatments
Impact on QoL
618
What features of MH are relevant to an ulcer history?
Previous medical diagnoses
Current medical problems
Is the patient attending any other hospital specialists
619
What are examples of systems of GI problems?
Weight loss
Constipation
Diarrhoea
Bloating
Reflux
Blood in stool
620
How does an aphthous ulcer present clinically?
Round/ovoid
Grey base
Erythematous halo
621
How does a minor apthous ulcer present?
Less than 1cm
7-10 days
Non-keratinised mucosa
No scarring
622
How does a major apthous ulcer present?
Greater than 1cm
Lasts > 2-3 weeks
Can affect all mucosa
Heals with scarring
623
How do herpetiform ulcers present?
Multiple tiny ulcers
Resemble herpetic ulcers
Can coalesce
Keratinised and non-keratinised surfaces
624
What investigations can be implemented for patients presenting with oral ulcers?
Blood tests- standard (fbc, haemantinics, coeliac screen), additional (ESR, ANA, viral screens)
Referral
Biopsy- to exclude ulcerative condition (+/- direct immunofluorescence
625
What conditions are associated with with Aphthous Like Ulceration (ALU)?
Behcet’s syndrome
Inflammatory bowel diseases
Gluten sensitivity enteropathy
Periodic fever, aphthous stomatitis, pharyngitis, cervical adenitis (PFAPA)
Haemantinic deficiencies
Zinc deficiency
Cyclic neutropenia and benign familial neutropenia
Primary and secondary immunodeficiencies (HIV)
Mouth and genital ulcers with inflamed cartilage (MAGIC syndrome)
Sweet’s syndrome
TRAPS (TNF receptor associated to periodic fever)
Food hypersensitivity
Drug reactions
626
What is Behçet’s disease?
Chronic relapsing multisystem inflammatory vasculitis
Affects large and small vessels
627
How does Behcets syndrome present?
Oral and genital ulcerations
Skin lesions
Uveitis
Inflammatory vascular involvement of the CNS and GIT
628
What is the International criteria for Behçet’s disease?
Ocular lesions- 2
Genital aphthosis- 2
Oral aphthosis- 2
Skin lesions- 1
Neurological manifestations- 1
Vascular manifestations -1
Positive pathology test- 1
629
What score on the International Criteria of Behçet’s disease is diagnostic?
>4
630
What is the first line of management for recurrent aphthous ulcers?
Diet
Trauma
Toothpaste
Topical- benzydamine, lidocaine, covering agent, chlorhexidine
631
What is the second line of management for recurrent aphthous stomatitis?
Topical corticosteroids (creams, gels, sprays, mouthwashes)- beclomethasone
Topical antibiotics - doxycycline
Consider vitamin b12
632
What is the second line of management for recurrent aphthous stomatitis?
Topical corticosteroids
Topical antibiotics
Consider vitamin b12
633
What instructions should be given to a patient who is prescribed doxycycline capsules for recurrent aphthous stomatitis?
Dissolve contents of capsule in 10ml water
Hold in mouth for 4 minutes over ulcers
Spit out
Do not rinse, eat or drink for 20 mins
634
What instructions should be given to a patient who is prescribed doxycycline capsules for recurrent aphthous stomatitis?
Dissolve contents of capsule in 10ml water
Hold in mouth for 4 minutes over ulcers
Spit out
Do not rinse, eat or drink for 20 mins
635
What are examples of holistic treatments for recurrent aphthous stomatitis?
Garlic
Coconut
Lavender oil
Aloe vera
Herbal remedies
Silver nitrate
Botox
636
What is the third line of management for recurrent aphthous ulcerations?
Corticosteroids
Colchicine
Pentoxyphilline
Thalidomide
Azathioprine
Mycophenolate
Biologics
637
What is the third line of management for recurrent aphthous ulcerations?
Corticosteroids
Colchicine
Pentoxyphilline
Thalidomide
Azathioprine
Mycophenolate
Biológicos
638
What does TUGSE stand for?
Traumatic ulcerative granuloma with stromal eosinophilia
639
What is TUGSE?
Rare, benign and self limiting form of oral ulceration
Uncertain aetiology (associated with complex MH, dry mouth and persistent oral ulcers)
Resolution after biopsy common
Topical/intra-lesional steroid tx may provide benefit
640
What medications/factors may be associated with TUGSE?
Cytotoxic drugs- methotrexate
NSAIDs
Nicorandil- potentially inhibits cell migration necessary to repair mucosal micro trauma
Age; co-morbidities; other medications
641
What should be avoided in the diet of patients with RAS
Benzoates
642
What is oral lichen planus?
An inflammatory condition of the mouth that may occur on its own or with skin, nail, or genital lichen planus. Affects 1-2% of the population, predominantly middle-aged and elderly women.
## Footnote
It can also affect men, but children are rarely impacted.
643
What is the cause of oral lichen planus?
The cause is largely unknown but likely related to the immune system. It is not an infection and is not contagious.
## Footnote
Some cases may link to chronic hepatitis C virus infection or certain medications and dental materials.
644
Is oral lichen planus hereditary?
It may have a genetic basis, but it is uncommon for multiple family members to be affected.
645
What are the symptoms of oral lichen planus?
Symptoms may include burning or stinging discomfort, especially with spicy foods, citrus fruits, and alcohol. Mild cases may be symptom-free.
## Footnote
Ulcers (erosions) can occur and cause significant pain.
646
What does oral lichen planus look like?
Typically presents as a white, lace-like pattern; can also appear as white and red patches or ulceration. Gum involvement is known as desquamative gingivitis.
## Footnote
This causes gums to appear red and shiny.
647
How is oral lichen planus diagnosed?
Diagnosis can often be based on appearance, but a biopsy may be needed for microscopic examination.
648
Can oral lichen planus be cured?
Generally, it cannot be cured but may resolve spontaneously. Treatments can help manage symptoms.
## Footnote
Changes in medications or dental materials may improve oral lichenoid lesions.
649
Is oral lichen planus serious?
It is usually not serious, but there is a small risk (about 1%) of cancerous change over 10 years.
650
What are the treatments for oral lichen planus?
Topical treatments include:
* Anaesthetic mouthwashes
* Topical steroids
* Topical tacrolimus
* Good oral hygiene practices
## Footnote
Systemic treatment may be required in severe cases.
651
What can patients do to manage oral lichen planus?
Patients should:
* Avoid spicy, acidic, or salty foods
* Maintain oral hygiene
* Use mild-flavored toothpaste
* Regularly see a dentist for check-ups
* Avoid smoking and limit alcohol intake.
652
Fill in the blank: Oral lichen planus affects primarily _______.
middle-aged and elderly women.
653
True or False: Oral lichen planus is contagious.
False
654
What are common triggers for discomfort in oral lichen planus?
Spicy foods, citrus fruits, and alcohol.
655
What is desquamative gingivitis?
Gum involvement in oral lichen planus that causes gums to become red and shiny.
656
What is the risk of cancer associated with oral lichen planus?
About 1% risk over a period of 10 years.
657
What are the systemic treatment options for severe oral lichen planus?
Oral corticosteroids, azathioprine, and mycophenolate mofetil.
## Footnote
Regular blood tests are required to monitor for drug toxicity.
658
What does saliva do?
Acid buffering
Mucosal lubrication- speech, swallowing
Taste fcailation
Antibacterial/fungal
Digestive
659
What are the causes of dry mouth?
Dehydration
Drugs
Age, Smoking, Alcohol
Radiotherapy and cancer treatment
Anxiety and Somatisation disorders
Salivary gland disease
660
What are the age related changes to salivary tissue between 17-90 years?
Acinar tissue loss (structural);
37% submandibular
32% parotid
45% minor glands
661
What are the age related changes to salivary tissue between 17-90 years?
Acinar tissue loss (structural);
37% submandibular
32% parotid
45% minor glands
662
What salivary glands are examined extra orally?
Major salivary glands
663
What saliva glands are examined intra orally?
Minor salivary glands
Duct orifices
Fluid expression
664
What saliva glands are examined intra orally?
Minor salivary glands
Duct orifices
Fluid expression
665
What developmental abnormalities are associated with dry mouth?
Agenesis
Atresia
Aplasia- ectodermal dysplasia
Hypoplasia
666
What developmental abnormalities are associated with dry mouth?
Agenesis
Atresia
Aplasia- ectodermal dysplasia
Hypoplasia
667
Which ectopic gland tissue disorders are associated with dry mouth?
Stafne’s bone cavity
Accessory parotid
Lymph node inclusions
668
How many people in Scotland carry the mutation for CF?
1 in 2000
Autosomal recessive inheritance- less than 20 cases per year
669
What does CF affect?
Exocrine glands
Duct plugging, calculi, atrophy
670
What drugs are associated with Drug Induced Salivary Hypofunction?
Amphetamines (ADHD)
Anticonvulsants (TN)
Antidepressant
Antihistamines
Antineoplastic drugs
Antiparkinsonian
Antipsychotics
Anti retrovirals
Diuretics (bendroflumethiazide 10% red)
Antihypertensives
Muscle relaxants
Opioid analgesics
Benzodiazepines
Anticholinegics (amitriptyline 26% red)
Lithium (70% red)
671
What aspects of radiotherapy and cancer treatment are associated with dry mouth?
Radiation effects (apoptosis then inflammation and fibrosis)
Graft vs host effects
Antineoplastic drugs
Radioiodine
672
What chronic systemic diseases are associated with dehydration and dry mouth?
Diabetes Mellitits
Renal/cardiac failure
Hypercalcaemia
Diabetes Insipidus
Addisons disease (hypovolaemia)
673
What acute systemic diseases are associated with dehydration and dry mouth?
Haemorrhage
Persistent vomiting
674
What other systemic conditions are associated with dry mouth?
Sarcoidosis
HIV associated salivary disease or drugs
Gland infiltration/destruction (amyloidosis)
675
What are the associations between anxiety and somatisisation disorders?
Cephalic control of salivation- inhibition of salivation
Celhalic control of perception- altered perception of reality burning mouth syndrome
676
What are the symptoms of somatisation?
Oral dysaesthesia
TMD pain
Headache
Neck/back pain
Dyspepsia
IBS
PTSD
Myalgic Encephalomyelitis (CFS)
Dysfunctional uterine bleeding
Chronic pelvic pain
Fibromyalgia
677
What is DISH?
Drug Induced Salivary Hypofunction
678
What autoimmune disorders are associated with dry mouth?
Sicca disease
sjogrens disease (primary- no connective tissue disease, secondary- connective tissue disease)
679
What is the aetiopathogenesis of sjogrens?
HLA association; DR3 and DR52
680
What are the eye symptoms of sjogrens?
Persistent troublesome dry eyes for >3 months
Recurrent sensation of sand/gravel in eyes
Tear substitutes used >3 times a day
681
What are the oral symptoms of sjogrens?
Daily feeling of a dry mouth >3 months
Recurrent swelling of salivary glands as an adult
Frequently drinking liquid to aid swallowing dry foods
682
How is a Sjogrens diagnosis confirmed as per BSR?
Anti-Ro antibodies - score 3 (blood test)
Focus score of > or = 1 - score 3 (gland biopsy)
Abnormal ocular staining score > or = 5 (score 1) (slit lamp examination)
Schirmers test without anaesthetic result < or = 5mm / 5min - score 1 (filter paper)
Unstimulated salivary flow < 0.1ml/min - score 1 (spit in cup)
Classification of SD requires a score of 4 or more
683
What is Anti-Ro Test?
Antibody in the blood against an extractable nuclear antigen (ENA)
High specificity and sensitivity for sjogrens
684
What is a focus score?
Positive labial gland biopsy - gold stat card test
50+ lymphocytes per 4mm2 of tissue, focus score > or = 1 translates to a score of 4 EULAR/ACR 2026 criteria
685
What is the histopathology of SD in minor glands?
Focal lymphocytic sialadenitis
Acinar loss
Fibrosis
686
What is the histopathology of SD in Parotid gland?
Lymphocyte infiltrate
Epithelial hyperplasia
687
How does the slit lamp examination work?
Lissamine- green/fluorescein to highlight corneal and conjunctival staining (keratocunjunctivitis sic a)
Scored 0-12
688
What is an abnormal result to a sialometry?
<1.5ml in 15
689
What are the ideal conditions for a sialometry?
Darkened quiet room
No talking or chewing
Allow saliva to gather then gently drool into container
No eating, drinking or smoking for 90 mins before
Measure over 5-15 mins
690
What are the ideal conditions for a sialometry?
Darkened quiet room
No talking or chewing
Allow saliva to gather then gently drool into container
No eating, drinking or smoking for 90 mins before
Measure over 5-15 mins
691
What are the head and neck complications of Sjögren’s syndrome?
Oral infection
Caries risk
Functional loss
Dentures retention
Salivary lymphoma - B Cell, NHL, 1-5% of long standing cases, unilateral gland size change
692
What factors consistently emerge as predictors of future lymphoma development in SD in adults and children?
Low C3/C4 with low C4 being strongest predictor
Clinical evidence of salivary gland enlargement
Clinical evidence of lymphadenopathy
Anti-Ro and or La and are
Cryoglobulinaemia
Monoclonal gammopathy
High focus score
693
How does sjogrens disease affect the systems?
CNS- fatigue, peripheral and CN neuropathies
Skin- xeroderma, rashes
Vascular— Raynaulds disease
Eyes- keratoconjunctivitis sicca, corneal ulcers
Respiratory- chronic cough/hoarseness
GI- dysphagia and pancreatic insufficiency
Haematological- anaemia and lymphopaenia
Musculoskeletal- myalgia, arthralgia
GU- vaginal dryness and dyspareunia
694
How is dry mouth assessed?
Gland palpation
Duct expression
Challacombe scale
Discriminating DISH from sjogrens- can you eat without a drink?
695
How is dry mouth managed?
Treat underlying cause- correct hydration, avoid caffiene, smoking and alcohol, modify drug regime , treat somatoform disorder
Preventive care
Symptomatic relief
Artificial saliva products
696
What does preventive care for management of dry mouth include?
Caries- diet, fluoride, treatment planning
Candida/staphlococci
Angular checking is (treat the reservoir first)
Sore tongue (sls free toothpaste)
697
What does the symptomatic relief for sjogrens include?
Sprays- glandosane. (pH 5.75), saliva orthana (contains porcine mucin), saliveze (pH neutral- carmellose), xerotim (SF, pH neutral)
Lozenges/pastilles- saliva orthana (contains porcine mucin),salicin (SF but acidic pH), saliva stimulating tablets (est- acidic pH), xylimelts
Salivary stimulants- pilocarpine (salagen)
Oral care systems/gels- biotene oral balance (lactoperoxidase, lysozyme), bio extra gel (similar to OB), xerostom
698
What simple lifestyle measures can relieve sjogrens?
Moist, oily foods/sauces
Humidify home environment
Regular exercise
Omega 3 supplements
Glasses/goggles to reduce tear evaporation
Warm compress on eyes 10 mins a day
699
What is associated with true hypersalivation/sialorrhea?
Stroke
Drugs
Degenerative CNS disease (MS CvJD, Alzheimer’s)
Parkinson’s
700
What drugs are associated with hypersalivation?
Parasympathomimetics
Buprenorphine
Anticholinesterases
Haloperidol
Clonazepam
Nicardipine
Clozapine
Ipecacuanha
Niridazole
Ammonium salts
bromides
Ethionamide
Iodides
Mercurial salts
Ketamine
701
What are the causes of perceived hypersalivation?
Swallowing failure- anxiety, stroke, motor neuron disease, ms
Postural drooling- cerebral plasy
702
What are the causes of perceived hypersalivation?
Swallowing failure- anxiety, stroke, motor neuron disease, ms
Postural drooling- cerebral palsy
703
How is hypersalivation managed?
Treat the cause
Drugs to reduce salivation- antimuscarinic agents
Biofeedback training- swallowing control
Surgery to salivary system- gland removal , duct repositioning
704
How is hypersalivation managed?
Treat the cause
Drugs to reduce salivation- antimuscarinic agents
Biofeedback training- swallowing control
Surgery to salivary system- gland removal , duct repositioning
705
What type of glands are salivary glands?
Exocrine
706
What nervous system is responsible for saliva control?
Autonomic nervous system
707
What is the role of the sympathetic division of the ANS in saliva?
Decreases salivary flow
Thoracic innovation
708
What is the role of the parasympathetic division of the ans in saliva?
Increases salivary flow
Cranial nerve innervation
709
What % of saliva is produced by major glands?
90%
710
What are the major salivary glands?
Parotid
Submandibular
Sublingual
711
What are the features of the parotid gland?
Parotid duct/ Stensens duct
Duct orifice in buccal mucosa in region of the upper first molars
Parasympathetic innervation from glossopharyngeal nerve
Intragland lymph node
712
What are the features of submandibular glands?
Submandibular duct/ whartons duct
Duct orifice in anterior floor of mouth
Parasympathetic innervation from facial nerve
713
What are the features of submandibular glands?
Submandibular duct/ whartons duct
Duct orifice in anterior floor of mouth
Parasympathetic innervation from facial nerve
714
What are the features of sublingual salivary glands?
Responsible for 7-8% saliva
Multiple ducts- some connect to submandibular duct
Parasympathetic innervation from facial nerve
715
What are the features or minor salivary glands?
800-1000
Labial, buccal and lingual mucosa
Hard and soft palate
1-2mm diameter
May have its own duct or shared with other surrounding glands
Lie beneath the mucosa or between muscle fibres
716
What are causes of salivary glands lumps/ swellings?
Obstruction
Sialodenitis
Sialosis
Neoplasm
Trauma and fluid
Solid deposits
Intragland lymph node swelling
717
Description and examples of salivary gland obstruction?
Something stopping saliva from leaving the gland
Salivary duct calculi
Duct structure
718
Description and examples of sialodenitis?
Inflammation of the salivary glands
Sjogrens syndrome
Infection
IgG4 syndrome
719
Description and examples of sialodenitis?
Inflammation of the salivary glands
Sjogrens syndrome
Infection
IgG4 syndrome
720
Descriptions and examples of sialosis?
Bilateral painless swelling
721
Descriptions and examples of neoplasm affecting salivary glands?
Malignant and non malignant tumours
Pleomorphic salivary adenoma
Warthins tumour
Mucoepidermoid carcinoma
722
Description and examples of trauma and fluid affecting salivary glands?
Oedema and blood
Trauma
Allergy
723
Description and examples of trauma and fluid affecting salivary glands?
Oedema and blood
Trauma
Allergy
724
Descriptions and examples of solid deposits affecting salivary glands?
Protein build up
Amyloidosis
725
Descriptions and examples of solid deposits affecting salivary glands?
Protein build up
Amyloidosis
726
Descriptions and examples of intra-gland lymph nodes swellings afffecting salivary glands?
Lymph nodes within the gland swelling
Lymphoma
Acute infection
727
What are the symptoms of obstructive sialadenitis?
Intermittent swelling of salivary glands
Usually unilateral
May or may not have inflammation
Usually painful but it can be painless
Often associated with mealtimes
May have accompanied bacterial sialadenitis
Can be chronically obstructed- may lead to gland atrophy
Most common in submandibular duct Parasympathetic innervation
728
What are the causes of obstructive sialadenitis?
Sialkot has- duct calculi- most common submandibular due to duct anatomy
Stricture in salivary duct
Salivary duct oedema- trauma
Neoplasm
Mucous plug
729
What questions should you ask when taking a history for suspected obstructive sialadenitis?
Pain history if needed
Ask if associated with eating/food
Coming and going or persistent
Swallowing problems
Bad taste or pus
Generally unwell- to exclude acute infection
730
What questions should you ask when taking a history for suspected obstructive sialadenitis?
Pain history if needed
Ask if associated with eating/food
Coming and going or persistent
Swallowing problems
Bad taste or pus
Generally unwell- to exclude acute infection
731
What % of saliva is produced by parotid?
20-25%
732
What is the clinical assessment for suspected obstructive sialadenitis?
Extra oral exam
Bimanual palpation of FoM
Express saliva from ducts
733
What is the clinical assessment for suspected obstructive sialadenitis?
Extra oral exam
Bimanual palpation of FoM
Express saliva from ducts
734
What investigations should be carried out for suspected obstructive sialadenitis?
Lower occlusal xray +/- opt to identify calcification
Ultrasound scan
Sialography
MRI or CT may be indicated
735
What are the conservative measures to manage obstructive sialadenitis?
Massage the gland and duct
Heat application
Sucking on citrus/fruits/sweets
Stay hydrated
Excellent oral hygiene
Simple analgesia
736
What is the surgical/radiological management of obstructive sialadenitis?
Lithotripsy
Sialoendoscopy
Balllon dilation
Basket removal
Incisional removal
Therapeutic sialogroahy
737
What are the complications of surgical/radiological management of obstructive sialadenitis?
Damage to duct
Displace stone into FoM or closer to gland
738
What the types of sialadenitis?
Acute viral sialadenitis- mumps
Acute bacterial sialadenitis
Chronic sialadenitis- Sjögren’s syndrome, sarcoidosis, IgG4 disease
739
What is the aetiology of acute viral sialadenitis?
RNA paramyoxovurus (mumps)
2-3 week incubation
Partiendo are infective a few days before and after parotid swelling
Highly infective, spreads by direct contact and saliva droplets
740
What are the clinical features of acute viral sialadenitis?
Painful parotid swelling
Usually bilateral
Can sometimes be a single gland
No hypo-salivation
10% have submandibular gland involvement
Very rare to involve only the submandibular gland d
Malaise, fever and feeling generally unwell
Trismus
Swelling lasts around 7 days
741
What are the clinical features of acute viral sialadenitis?
Painful parotid swelling
Usually bilateral
Can sometimes be a single gland
No hypo-salivation
10% have submandibular gland involvement
Very rare to involve only the submandibular gland d
Malaise, fever and feeling generally unwell
Trismus
Swelling lasts around 7 days
742
What are the complications of acute viral sialodenitis?
Extra salivary manifestations- orchid is (25%), oophoritis (5%), thyroiditis, pancreatitis,meningoencephalitis deafness in 1in 3400
Nervous system- meningitis (headache, photophobia, neck stiffness) 15% cases, meningitis and encephalitis can occur
743
How is acute viral sialadenitis diagnosed?
Clinically
Serum antibodies can be considered
Viral swab of saliva
744
How is acute viral sialadenitis managed?
Supportive therapy- hydration, analgesia, pyrexia management, isolated for 6-10 days may be advisable, contact public health
745
How is acute viral sialadenitis prevented?
Two doses of MMR vaccine before age of 5
Confers a 61-91% protection after two doses for mumps and d99% against measles and rubella
746
What are the features of acute bacterial sialadenitis?
Most common in parotid glands
Typically unilateral
Painful swelling
Overlying erythema
Pus from duct
Trismus
Pyrexia
Cervical lymphadenopathy
Often secondary to salivary gland obstruction
747
What are the risk factors of acute bacterial sialadenitis?
Dehydration
Radiotherapy
Duct obstructions
Sjogrens disease
Poor oral hygiene
Smoking
748
How is acute bacterial sialadenitis diagnosed?
Clinically
Excluded odontogenic infection- consider opt
Pus swab for culture and sensitivities often caused by streptococcus viridans and staphylococcus aureus
Exclude pyrexia/sepsis
Exclude airway obstruction- contact emergency/OMFS for advice
May need inpatient support/management
749
What is the management of acute bacterial sialadenitis?
Antibiotics through GP or OMFS
First choice is flucloxacillin, erythromycin in penicillin-allergic patients
Airway management if needed
Manage causative factors
750
What is sialosis?
Benign and bilateral salivary gland hyperplasia
Painless
Soft
Associated with autonomic neuropathy
751
What is sialosis associated with?
Alcohol excess
Endocrine disorders- diabetes, acromegaly
Malnutrition
Anorexia
Bulimia
Cystic fibrosis
Cirrhosis
752
What investigations may be carried out for suspected sialosis?
Hba1c/LFt may be considered
Ultrasound scan to exclude other conditions eg sarcoidosis or warthins tumour
Rarely sialography or core biopsy
753
Why are examples of systemic causes of salivary gland swellings?
Sjogrens disease
IgG4 disease- recently reorganised, rare autoimmune condition that can affect most organs
Sarcoidosis- rare mulisystem non-caseating granulomatous reaction, lung involvement in 90% patients
754
What symptoms associated with salivary swelling should make you consider onward referral?
Shortness of breath
Cough
Chest pain
Uveitis
Macroglossia
Peripheral neuropathy
Bruising/purpur
Peripheral oedema
GI symptoms
Fatigue
Weight loss
755
What is a mucocele?
Cystic lesion of the minor salivary glands
756
Where are mucoceles usually present?
Lower labial mucosa
FoM
Rare in upper lip but higher malignancy risk if so
757
How do mucoceles appear?
Fluctuant
Blue swelling
Swelling
758
What are the types of mucoceles?
Mucous extravasation
Mucous retention
759
What is mucous extravasation mucoceles?
Caused by trauma to the minor salivary duct (90% of mucoceles)
Not lined by epithelia therefor not true cyst
May have mucin and inflamed granulation tissue histologically
Most commonly present in the lower lip /labial mucosa (70%)
Floor of mouth occurence is a ranura
Most commmon under 30 peak incidence in 2nd decade
760
What are the features of mucous retentive mucoceles?
Saliva being retained in duct/gland (10%)
More common over the age of 50
Here seen on lower lip
Cystic dilation of the duct
761
What are the features of a history of a mucoceles?
Swelling
Rupture
Partially resolution
Recurrent e
History of trauma/biting
762
What is the management of mucoceles?
No treatment- unlikely to resolve
Excision by oral surgery- ideally enucleation (high recurrence)
Clinical photos
763
How does necrotising sialometaplasia present?
Swelling then ulceration
Usually painless, self healing
A
764
What are differential diagnoses to necrotising sialometaplasia?
Squamous cell carcinoma
Salivary gland carcinoma
765
What is the aetiology of necrotising sialometaplasia?
Small vessel infarction/ischaemia
Smokers/trauma and La
766
What is the histology of necrotising sialometaplasia?
Surface slough
Hyperplastic surface epithelium
Squamous metaplasia of the ducts
Necrosis of salivary acini
767
What are the features of neoplasms?
Mainly benign
Salivary neoplasms uncommon
Usually present as unilateral parotid swelling s
Pleomorphic adenomas most common
Malignancy most common in minor salivary glands
768
What are examples of benign salivary neoplasms?
Pleomorphic adenoma
Warthin tumour
Myoepithelioma
Basal cell adenoma
Oncosytoma
Canalicular adenoma
769
What are examples of malignant salivary neoplasms?
Acidic cell
