oral med Flashcards
keratosis
keratin formation in non-keratined sites
acanthsosis
hyperplasia of stratum spinosum
elongated rete ridges
due to
basal cell hyperplasia
atrophy
thinning of normal epithelium
reduction in viable cell layers
erosion
partial thickness loss of epithelium
ulceration
full thickness loss of epithelium
oedema
fluid accumulation and swelling
intracellular or intercellular (spongiosis)
blister
localised accumulation of fluid
vesicle <0.5mm
bulla >0.5mm
causes of chemimcal burns
drug induced (aspirin burns)
ingestion of bleach/strong acid
differential dx for white patch
heriditary
frictional keratosis
chemical burn
smoking kertosis
systemic lupus erythematous
chronic hyperplastic candidosis
squamous cell carcinoma
leukoplakia
lichen planus
heridatary white patches
2
white sponge naevus
fordryces spots/granules
white sponge naevus
features
heridatrary
diffuse
asymptomatic
soft unevening thickening of surface epithelium
often on non-keratinised mucosa
widespread oedema
fordyce spots
visible inactive sebaceous glands
small, raised, white/pale pink spots/bumps 1-3mm in diameter
usually around vermillon border, buccal mucosa, gentials
management of heriditrary white spot lesions
reassurance that is it not cancer
if any symptoms (unlike) advice on relief
causes of frictional keratosis
response to chronic low grade trauma
e.g.
* sharp cusps/restorations
* ill fitting denture
* cheek biting (parafunction)
clinical appearnce of frictional keratosis
white patch surrounded by erythematous inflammation
caused by reactive thickining of mucosa
histology of frictional keratosis
epithelial hyperkeratosis
acanthosis - hyperplasia of stratum spinosum
variable dysplasia
minimal infiltrate
how to manage frictional keratosis
remove souce (adjust denture, trim cusp/restoration, provide splint)
review
if no sign of healing within 2 weeks - urgent biopsy required
smokers keratosis
low grade burn and chemical irritation
usually on palate
smokers keratosis clincial appearnance
painless white keratotic layer
presence of small red spots (blocked sebaceous glands)
histology of smokers keratosis
hyperkeratosis
variable dysplasia
minimal infiltrate
underlying melanin pigmentation
management of smokers keratosis
smoking cessation
leukoplakia defintion
white patch which cannot be rubbed off or attributed to other cause
dx of exclusion
lichen planus histology
hugging band of T lymphocytes (cell mediated)
change in surface epithelium (hyperkeratosis/atrophy)
civatte bodies (apoptosed intraepithelial cells)
basal cell liquefaction
saw tooth retet ridges
risk of malignant transformation of lichen planus
1-5%
types of lichen planus
6
Reticular
Atrophic
Ulcerative/Erosive
Bullous
Plaque
Papular
erythroleukoplakia
Mixed red and white paatch
erythoplakia management
urgent biopsy
high chance of malignant potential
erythroplakia
red patch which cannot be rubbed off or attributed to any other cause
needs urgen biopsy
causes of pigmentation
internal
racial pigmentation
reactive melanosis/melanotic macule (freckle)
melanoma
systemic conditions - haemosiderin; impetigo
causes of pigmentation
internal
- racial pigmentation
- reactive melanosis/melanotic macule (freckle)
- melanoma
- systemic conditions - haemosiderin; impetigo; ADDISONS; Peutz-jejgers syndrome
- pigmentary incontinence
- kaposis sarcoma
causes of pigmentation
extrinsic
- tea,coffee,CHX
- bacterial overgrowth
- metals - amlagam
- smoking
macule appearance
usually solitary
<1cm in diameter
well defined
flat border
commonly lower lip, freckle like
melanocytic naevus
appearance
management
common on vermillon border and palate
can be >1cm
no change in size or colour
monitor, biopsy if concerned
reassure and review
syndromes associated with multiple naevi
2
peutz-jehers syndrome
* benign polyps in GIT and multiple small peri-oral naevi
gorlin-goltz syndrome
* multiple odontogenic Keratocysts and basal cell carcinomas
kaposi sarcoma is linked to
HHV-8 and HIV2
clinical appearnce of kaposis sarcoma
red/purple
individual or groups
flat or raised, slow progression
risk factors for kaposi sarcoma
immunosuppression
chronic lympodema
management of kaposi sarcoma
biopsy
surgery
radio and chemotherapy
biologics
HAART
clinical red flags for malignant melanoma
- change in size, shape, colour (very dark)
- itchy
- skin breakdown
- bleeding
causes of oral malignant melanomas
unknown/idiopathic
UV on skin of lips
secondary melanosis
* smoking
* drug related
* inflammation
* addisons disease/adrenal insufficiency
drugs which can lead to infection
- antifungals
- steroids
drugs linked to licheniod reactions
- ACE inhibitors
- beta blockers
- diuretics
- nifidepine
- NSAIDs
- anticonvulsants
- omeprazole
- tetracycline
- oral hypoglyceamics
- antimalarias
drugs which can cause ginigval hyperplasia
- phenytoin
- cyclosporin A
- nifidipine
drugs which can cause oral pigmentation
antimalaraias
phenothiazines
hydroxychloroquinone
CHX
OCP
cisplatin
drugs which can cause oral pigmentation
antimalaraias
phenothiazines
hydroxychloroquinone
CHX
OCP
cisplatin
drug which can cause characteristic oral ulceration
nicorandil - angina
large, deep, persistent ulcers that have punched out edges
haemagioma
benign vascular tumour derived from blood vessel cell types
types of haemangioma
cavernous
capilllary
cavernous haemangioma
larger
encapsulated
dilated vascular space
capillary haemangioma
not encapsulated
thin walled capillaries
sturge weber syndromes
associated with vascular malformation
port wine stain that runs in distribution of CNV
lymphangioma
malformation of lymphatic system characterised by thin walled cyst lesion
commonly <2yrs old
geographic tongue
common, benign, inflammatory condition
1-2% adults
unknown aetiology
rapid appearance and disappearance, can change
areas of atrophic (red) and white keratotic areas with demarcated borders on dorsal surfaces of tongue with temporary loss of filiform papullae (depapillation)
clinical appearnce of geographic tongue
areas of atrophic (red) and white keratotic areas with demarcated borders on dorsal surfaces of tongue with temporary loss of filiform papullae (depapillation)
management of geographic tongue
dietary avodiance (hot,spicy foods, SLS)
sytomatic relief - benzydamine mouthwash
histology of geographic tongue
central lesion erosion and hyperkeratosis
chronic inflmmatory cells underlying connective tissue
causes of glossitis
vitamin/nutritional deficiencies
haematological deficiencies
clinical appearance of glossitis
loss of papullae
smooth red shiny dorsal surface
lobulated if severe
beefy tongue if haemaotological cause
management of glossitis
correct any underlying def
symptomatic relief
s
coated tongue
causes
management
build up of normal cellular debris on dorsal surface
dehydration, illness, poor diet
removal with abrasive instruement
correct underlying cause
possible tissue conditions due to dentures
chronic erythematous candidosis
leaf fibroma
papullar hyperplasia
osteogenesis imperfecta
type 1 collagen defect
features: blue sclera; weak bones; multiple easy fractures; dentinogenesis imperfecta
pathophyisiology of osteoporosis
bone atrophy - resorption occurs more than formation leading to endosteal net loss (quantitis deficiency)
bone consequence of hyperparathyroidism
osteitis fibrosa cystic (brown tumour)
giant cell lesion within the bone (bone swelling)
will regress if hyperparathyroidism is appropriately treated
histological appearance of hyperparathryoid bone lesions
multinucleated giant cells
haemosiderin
cystic cavities
osteitis fibrosa cystica (brown’s tumour)
primary herpetic gingivostomatitis
clinical features
widespread shallow vesicles - burst to form ulcers
gingival erythema
fever, malaise, halitosis, enlarged tender lymph nodes
primary HSV infection
primary herpetic gingivostomatitis
clinical features
widespread shallow vesicles - burst to form ulcers
gingival erythema
fever, malaise, halitosis, enlarged tender lymph nodes
primary HSV infection
management of primary herpetic gingivostoomatisis
self limiting
benzydamine spray
bed rest
analgesia
fluids
if child unable to eat/drink - hospital
pathogenesis of recurrent HSV
reaactivation of primary infeciton which is belived to lie dormant in dorsal root of trigeminal ganglia CNV3
oral presentation of recurrent HSV
herpes labalis - crop of blisters on lip
causes of recurrent HSV activation
trauma
sunlight
stress
immunocompromised/illness
disease progression of HSV
prodromal phase - burning/tingling
3-4 days before cold sore appearnce
management of HSV
High dose acyclovir during periods of acute infection (cream during prodromal phase),
long term low-dose acyclovir (prophylactic)
fluids, analgesia
varicella zoster virus
what are clinical presentations
Varicella - primary infection (chicken pox)
Zoster - reactivation of latent virus from sensory ganglion (shingles)
clinical appearance of varicella
Centripetal rash, fully body cutaneous spots, itchy, prone to bleeding
chickn pox
clinical appearance of zoster
Confined to distribution of nerve it remains dormant in.
Unilateral lesion, never crossing midline, sometimes CN V.
Painful vesicles, rupture to ulcers, crusting, scarring, pigmentation
EBV causes
clinical appearance
infectious mononucleosis
sore throat, generalised lymphadenopathy, fever, headaches, malaise, maculopapular rash
group A coxsackie causes
2
herpangina
hand, foot and mouth disease
clinical appearance of herpangina
wide spread small (pinhead) ulcers on uvula, palate, fauces
fever
sore throat
conjunctivitis
coxsackie group A
clinical appearance of hand, foot and mouth disease
papular, vesicular rash on hands and feet
oral vesicles which rupture into superficial painful ulcers (widespread, pinhead)
like herpangina but hands and feet affected too
coxsackie group A
EBV herpes number
4
syphillis appearance
primary secondary tertiary
Chancre - painless ulcerated nodule at site of inoculation, cervical lymphadenopathy
Cutaneous rash, condylomata, sensitive sloughy mucosa, serpiginous ulceration, malaise, fever, weight loss
Gumma - necrotic granulomatous reaction, enlarges and ulcerates, multi system disorder
how does oral candidosis occur
disease of diseased
Altered regulation of oral microflora, some commensal organisms eradicated allow others to flourish, overgrow and become pathogenic
examples of candidal species
c.aureus
c.albicans
c.tropicalis
c.krusei
c.glabrata
virulence factors for candida
hyphae
adherence
extracellular enzymes
stain needed for candida
PAS
doesnt show up well on H&E
types of candidosis
5
acute pseudomembranous
chronic erythematous
chronic hyperplasia
chronic atrophic
chronic mucocutaneous
acute pseudomembranous candidiosis appearance
white plaques, lightly adherent, can be rubbed off, discomfort eating, burning sensation, bad taste
clinical appearance of erythematous candidosis
atrophic mucosa, shiny red appearance
causes of pt becoming suscpetible to candida infection
denture
antibiotic stomatitis
indwelling cather
dry mouth/smoking/polypharmacy
post surgery
clinical appearance of chronic hyperplastic candidiasisi
white, nodular patches
on buccal mucosa, dorsum of tongue or oral commisures
unilateral or bilateral
biopsy - PMD
denture induced stomatitis
term
chronic erythematous stomatitis
wide spread erythema on mucosal surfaces underlying denture fitting surface
asymp or burning sensation/bad taste
denture induced stomatitis
term
chronic erythematous stomatitis
wide spread erythema on mucosal surfaces underlying denture fitting surface
asymp or burning sensation/bad taste
tx of chronic erythematous stomatitis denture induced
denture hygiene advice
topical antifunglas - miconazole or nystatin
CHX Mouthwash
reline or remake denture
classification of chronic erythematous candidiasis
Newtons
3 types
type I - localised inflammation
type 2 - diffuse erythema
type 3 - granular inflammation
example of chronic atrophic candidosis
median rhomboid glossitis on tongue
flat midline area on dorsal posterior area of tongue
nodular, red/pink depapillation
pathogens involved in angular cheilitis
staphlycoccus aureus
candida albicans
angular cheilitis appearnce
red cracked skin at angles of mouth
causes of angular cheilitis
inadqequate denture vertical dimension
trauma
vitamin def (iron, B12)
dx for candida by
oral swab for angular cheilitis
oral rinse for intra oral
antifungal types
Polyenes - nystatin
Azoles - fluconazole
polyene antifungal
mech of action
Directly target ergosterol in cell wall, causing perforation and leakage of intracellular contents
nystatin
polyene antifungal
mech of action
fungicidal
Directly target ergosterol in cell wall, causing perforation and leakage of intracellular contents
nystatin
azole antifungal
mech of action
fungistatic.
Target ergosterol in cell wall by interrupting activity of enzyme involved in its production, 14a demethylase. risk of resistance (krusei and glabrata are naturally resistant)
micronazole, fluconazole
how common in minor RAU
up to 25% population
minor RAU characteristic
small <5mm
1-20 in crops of ulcers
non keratinised mucosa
red halo surrounding yellow fibrin base
heal within 1-2 weeks without scarring
commonly recur
how common is major RAU
10% of all RAS
characteristics of major RAU
> 10mm in diameter
oral or irregular, red halo with yellow fibrin base
<5 per crop
keratinised or non mucosa
scar on healing
take longer to heal (6-12 weeks)
how common is herpetiform RAU
5% of all RAU
clinical appearance of herpetiform RAS
<5mm
round or oral often coincide with larger ulcers
1-200 per crop
non- keratinising mucosa
heal in 1-2 weeks without scarring
bechets ulcers
numerous oral uclers
part of multisystem ulceration/pathology auto immune
managment of Bechets
MDT (derm, OM, rheum, ophth, etc.).
Symptomatic relief, sometimes anti-TNF therapies
causes of RAU
genetic - Bechets, SLE, erythema multiforme
nutritional def - haem
systemic disease - GI, AIDs
endocrine imbalance - pregancy
immunocompromised - HSV recurrent
environmental
allergy
4 types of hypersensitivity reaction
Type I - IgE mediated
Type II - cytotoxic
Type III - immune comple
Type IV - cell-mediated
examples of local immunological oral diseases
recurrent aphthous stomatitis
lichen planus
OFG
SLE
systemic immunological diseases with oral manifestation
erythema multiforme
sjoregns
SLE
systemic sclerosis
pemphigus
pemphigoid
methods of dx immune mediated diseases
biopsy for histological analsysis
direct immunofluorescence
vesicle
<5-10mm diameter
bullae
> 5-10mm diameter
dermatits herpetiformis is associated with
gluten sensitivity
examples of vesiculobullous diseases
pemphigoid
pemphigus
angina bullos haemorrhagica
linear IgA disease
dermatitis herpetiformis
epidermolysis bullosa
what is angina bullosa haemorrhagica
formation of blood blosers in the absene of trauma
palate
desquamative gingivitis
clinical descriptive term for full thickness gingivitis
often with clear distincition between inflamed and non inflamed mucosa
desquamative gingivitis
seen in
erosive lichen planys
mucous membrane pemphigoid
pemphigus vulgaris
erythema multiforme
SLE
erythema multiforme
type of hypersensitivity reaction
aetiology
type III
idiopathic
50% have trigger - drugs (NSAIDs, carbmazepine, penicillin), infection, pregnancy, UV, chemicals
erythema multiforme
appearance
target lesions - concentric erythemaotus rings on palms, legs, face, neck, lips, anterior mouth
crops of bullae, burst to ulcers
crust and heal in 2 weeks
fever often
management of erythema multiforme
self limiting
steroids
aciclovir
fluids
analgesia
erythema multiforme associated with
Stenven Johnson syndrome
clinical appearnce of pemphigoid
thick walled blisters
can be fluid or blood filled
full epidermis (sub-epithelial split)
types of pemphigoid
3
mucous membrane
cicatricial
bullous
aetiology of pemphigoid
autoimmunity against hemidesmosomes in basal cell layer
possible complications of cicatricial pemphigoid
scarring of eyes - can cause blindness or other ocular damage
(symblepharon)
histopathology of pemphigoid
sub epithelial antibody attack
* demoglein destroyed by antibodies
HEMIDESMOSOMES targeted
* loss of attachment between basal cell layer and underlying lamina propria
space gets filled with fluid
full thickness separation of epithelium
direct immunofluorence of pempigoid
linear
IgG and C3 often present in basement membrane
tx for pemphigoid
refer
steroids and immunomodulators (azathioprine)
pemphigus types
vulgaris
IgA
familia benign chronic
foliaceus
pathogensis of pemphigus
formation of autoantibodies (IgG, C3) against DESMOSOMES involved in cell-cell adhesion (dsg-1, dsg-3)
causing intra-epithelial separation above basal cell layer
clinical appearance of pemphigus
oedema
intra-epithelial blisters
rupture to leave white friable mucosa
red erosive areas
histological features of pemphigus
desmosomes target at periphery of spinous cell layer - INTRA EPITHELIAL split (supra basal)
tzank cells
acanthosis
direct immunofluorescence appearnce of pemphigus
basket weave appearnce
tx for pemphigus
refer
systemic steroids
azathriopine
ritzimab (biologics)
risk of maligannt transformation with leukoplakia
under 5%
hsitological predictors/features of mlaignant change
3
epithelial dysplasia
architectural changes - abnormal maturation and stratification
cytological abnormalities - cellular atypia
hsitological predictors/features of mlaignant change
3
epithelial dysplasia
architectural changes - abnormal maturation and stratification
cytological abnormalities - cellular atypia
dysplasia
disordered maturation of tissue (growth)
grades of dysplasia
epithelial hyperplasia
mild
moderate
servere
carcinoma in situ
WHO 2005
mild dysplasia features
chnages in lower third of epithelium
mild celllular atypia
moderate dysplasia features
changes in middle third of epithelium
moderate cellular atypica
severe dysplasia
changes in upper third of epithelium
severe cellular atypia
signs of cellular atypia
hyperchromatism
pleomorphism
change in size/number
mitotic bodies in epithelium, not just in basal layer
features of carcinoma in situ
malignant but not invasive - abnormal architecture, pronounced cytological atypia
histological features of dysplasia
7
- increased and abnormal mitotic bodies (higher position, abnormal form)
- nuclear and cellular pleomorphism (different size and shape),
- abnormal keratinisation (below normal keratin layer, keratin pearls),
- nuclear hyperchromatism - prominent and enlarged nuclei
- basal cell hyperplasia - elongated/drop shaped rete ridges
- distrubed basal cell polarity/loss of cellular orientation
- irregular epithelial startification or distrubed maturation
- reduced/lost intercellular adhesion
high risk sites for oral cancer
lateral border of tongue
FoM
retromolar areas
soft palate
risk factors for oral cancer
- smoking - cigarette, betel quid
- alcohol (synergistic with smoking)
- previous SCC
- first degree relative with OSCC
- poor diet
- low socioeconomic status
- viruses - HPV 16+18, EBV
- poor OH
6 hallmarks for carcinogenesis
o evading apoptosis
o self-sufficient in growth signals
o insensitivity to anti-growth signals
o sustained angiogenesis
o limitless replication potential
o tissue invasion and metastasis
cancer genetics
Molecular basis of cancer
* damage - inactivated, useless or over/under express
* altered gene expression - Gene responsible for protein which has a function
* altered cell function - if gene expression is changed and target for protein (function) is changed causes alteration in cell function
Oncogenes e.g. tumour suppressor genes (p53 mutation/inactivation)
* aneuploidy, translocation, amplifications
dysregulation of apoptosis and DNA repair
field change theory for tissue - not just PML
red flags for OSCC
- persistent (>2wk) ulcer despite removal of obvious cause,
- rolled margins,
- necrotic (firm) centre (indurated, inflamed, granular base, raised edges),
- speckled leukoplakia/non-homogenous
- weight loss,
- dysphagia,
- worsening pain (neuropathic, dysaesthesia, paraesthesia),
- referred pain (ear, throat, jaw),
- cervical lymphadenopathy (enlarged >1cm, firm, fixed, tethered, non-tender)
histological patterns for OSCC invasive front
4 types; 2 fronts
- Local,
- perineurial,
- lymphatics,
- haematogenous (lungs, spine, bone).
Cohesive or non-cohesive front (linked with nodal spread)
factors for OSCC prognosis
7
- Site,
- size,
- depth of invasion,
- disease spread,
- comorbidities,
- neck metastasis (contralateral and unilateral),
- extra capular spread
TMN staging
T - tumour
M- metastasis
N - nodes
T stages
T1 - <2cm
T2 - 2-4cm
T3 - >4cm
N stages
N0 - no clinically positive nodes
N1 - single ipsilateral node <3cm
N2 - single ipsilateral node 3-6cm or multiple nodes <6cm
N3 - any node >6cm
M stages
M0 - no distant mesatasis
M1 - distantn mesatasisi
OSCC management options
Resective surgery,
radiotherapy,
chemotherapy,
radiochemothearpy
immunotherapy
Curative intent, palliative, best-supportive care
possible causes of neck lumps
6
- head and neck cancer
- infection/reactive - abscess, pericoronitis, tonsilitis, glandular fever
- lymphoma
- skin swellings
- arterial (carotid aneurysm)
- bone issue
clinical presentation of reactive lymph nodes
large (diffuse)
tender
inflammed
erythematous surface
soft
mobile
hot
clinical presentation of metastatic nodal disease
large
firm
fixed/tethered to underlying tissue
clinical presentation of lymphoma nodes
large
rubbery
tethered
aetiology of lichen planus
Chronic immunological, cell-mediated (type IV) reaction.
Autoimmune condition mediated by a T lymphocyte attack on stratified squamous epithelium
commonly affected intra oral sites for lichen planus
buccal mucosa
gingivae
tongue (dorsal/ventral)
lips
skin lichen plnaus
itchy lesions (shiny red/purple papules)
interlaced by wickham’s straie (white lacy lines) on flexor surfaces
lichenoid reaction
known cause
e.g. amalgam, medications (ACE inhibitors, b-blockers, NSAID, diuretics, nifedipine)
reticular lichen planus
bilateral on buccal mucosa
white lacy like lines, spider web appearance
erosive (ulcerative) lichen planus
oral ulcers,
presistent irrgeular areas of erythema
assoc with desquamative gingivitis
papular lichen planus
small white asymptomatic pinpoint papules
palque lichen planus
large homogenous white pathces
resembles leukplaksia
common in smokers
palque lichen planus
large homogenous white pathces
resembles leukplaksia
common in smokers
atrophic lichen planus
common to erosive
atrophic lesions on backgound of eythema with radiating white striae at margins
bullous lichen planus
rarer.
Fluid-filled vesicles (white or grey/purple, fluctuant) that rupture easily, leave ulcerated surface.
Fluid is usually clear but may be haemorrhage or purulent
histology of lichen planus
5
- Keratinisation/keratosis of surface epithelium (hyperkeratosis - usually orthokeratosis),
- acanthosis (hyperplasia of underlying epithelium, especially spinous cells) - elongated rete ridges with saw-tooth appearance,
- thick sub epithelial ‘hugging’ band of T lymphocytes (blue band of chronic inflammatory cells under epithelium and following contour),
- occasionally epitheliotropism (inflammatory cells drawn up into epithelial layer),
- apoptosis (of basal cell layer - cells surrounded by clear halo),
- destruction of basal cell layer
lupus
what is it
types
connective tissue autoimmune disease
SLE (mutisystem), chronic discoid (limited to skin and mucosa)
clinical appearance of SLE
skin leasiosn - butterfly zygomatic rash
oral mucosal lesions (palate - ulcers, purport, red/white striae)
antinuclear antibodies
arthritis
anaemia
may have disc like white plaues intra orally
need topical steroids and disease modifying drugs
OFG hypersensitivty reaction
Type IV (sometimes type I) hypersensitivity to food additives; unknown aetiology.
pathogensis of OFG
Characterised by non-caseating granulomatous inflammation.
Lymphatic obstruction from giant cell granulomas, accumulation of tissue fluid
difference between OFG and Crohns
if systemic symptoms more likely to be crohns
clinical fearures of OFG
7
- Angular cheilitis,
- buccal mucosa cobblestoning,
- mucosal tags,
- aphthous-pattern ulceration (or other types) - esp linear in depth of buccal sulcus
- swollen lips, cheeks and gingivae (full-width gingivitis),
- gingival erythema,
- FoM oedema - stag horning
histology of OFG
4
- non caseating granuloma formation
- giant cell formation
- inc tissue fluid production between Connective tissue - causing separation of connective tissue
- lymphatic obstruction and oedema fluid build up
dx and managment of OFG
dx of exclusion
* allergy past test
* test for coelic - blood tests transglutaminase, faecal calprotectin
try dietary exlusion - cinnamon aldehyde, SLS, benzoates
steroids, disease modifying drugs, biologics, anti-TNF therapies
types and pathogenesis of Pagets disease
monostotic or polystotic
maxilla in pagets disease due to over activation of osteoclasts and osteoblasts
* Paget’s disease 3% of routine autopsies
* Mainly inc age and male
replacement of normal bone by remodelling by a chaotic alteraion of resorption and deposition
* causes inc bone
symptoms of paget’s disease
often asyptomatic
frontal bossing (dentures and hat no longer fit)
headaches
hearing disturbance
radiographic appearance of pagets disease
Cotton wool appearance
hypercementosis of teeth
histology of pagets
increased bone turnover so osteoclastic and osteoblastic activity
fibrous dysplasia
what it is
symptoms
slow growing asymptomatic swelling
active in those <20years
area of bone replaced by fibrous connective tissue
mono or polystotic
fibrous dysplasia
what it is
symptoms
slow growing asymptomatic swelling
active in those <20years
area of bone replaced by fibrous connective tissue
mono or polystotic
radiographic appearance of fibrous dysplasia
orange peel/ground glass appearance
ill defined margins between affected and unaffected bone
histology of fibrous dysplasia
bone appears metaplastic or woven but will remodel and inc in density
fibrous dysplasia associated with
Albright syndrome
- melanotic navi
- odontogenic keratocysts
- fibrous dyplias
- early puberty
causes of dry mouth
Polypharmacy/drugs, alcohol, smoking, radiotherapy, chemotherapy, poorly controlled diabetes, Sjogren’s, psychogenic
dx of dry mouth
unstimulated salivary flow rate <1.5ml in 15mins
issues dur to dry mouth
swallowing issues
issues in speech
dyseasethesia/pain or brunding mouth
alteraed taste
non retentive dentures
inc dental disease - caries, perio
halitosis
mucocele
swelling, bluish translucent colour, soft/fluctuant
can be mucous extracastaion or retention cyst
due to trauma to duct or minor salivar gland
common sites for mucoceles
lower lip
palate
buccal mucosa
tongue
FoM - ranula
histology of mucocele
cystic cavity containing saliva, wall of granulation tissue, macrophage lining
tx for mucocele
excision with damaged gland and duct
types of sjogrens
primary - no associated CT disease
secondary - associated with CT disease (e.g. SLE, RA, systemic sclerosis)
dx criteria for sjorgrens
modified european - 4+ crieteria (inc 5 or 6)
1 and 2. Dry eyes subjective/objective - dry for >3mths, recurrent sensation of gravel in eyes, tear substitutes >3 times/day
3 and 4. Dry mouth subjective/objective - for >3mths, reduced unstimulated flow rate, liquid to swallow dry food
5-Anti-Ro, anti-La autoantibodies (bloods)
6- Positive labial gland biops
histological features of sjorgrens
- more than one duct with 50+ lymphocytes (llymphocytic foci)
lymphotcytes cause
* acinic atrophy
* hyperplastic ductal epithelial
consequences of sjogrens
caries
oral infection
poor Oral healthy QoL
management of sjorgrens
sugar free gum
regular sips water
high F toothpaste
salivary substituties - biotene oral balance
sicca syndrome
dry mouth only
partial sjogrens
subacute obstruction
swelling associated with meals, slowly progressive and then eventually fixed and paiful
due to sialoliths or muccous plugs
causes of hypersalivation
stroke, MS , Parkinsonos, perceived
sialenditis
inflammation of major salivary gland
due to obstruction (stone, stricture) or bacterial (s.aureus)
removal obstruction, FNA and ABX, gland removal
sialenditis
inflammation of major salivary gland
due to obstruction (stone, stricture) or bacterial (s.aureus)
removal obstruction, FNA and ABX, gland removal
parotiditis
Bacterial infection, common in children, resolves by puberty
Freye’s syndrome
tx
syndrome involving duct and gland fistula (EO saliva leakage)
Botox, excision of duct, gland removal, propantheline before food (reduce salivary flow), scolopaline patches
sjorgen
sialograpy
US
snowstrom due to destruction of acini
leopard spot on US
US as no radiation
salivar gland most likely to get neoplasma
and % malignant
parotid 80% (15% malignant)
neoplasma in salivary gland
likelihood of lockation
parotid 80% (15% malignant)
submandibular 10% (30% malignant)
minor 10% (45% malignant)
sublingual 0.5% (80% malignant)
salivary gland neoplasma symptoms
localised swelling, painless
slow growing
well defined
neuro changes (CNVII involved)
most common neoplasm is salivary gland
pleomorphic salivary adenoma (75%)
histological features of pleomorphic salivary adenoma
2
incomplete capsule
foam cells (macrophages that have engulfed mucin)
mixed
management of PSA nad issues
wide local excision
high recurrnece - due to incompleted capsule
5% risk of maligannt
Warthin tumour
most commonly parotid
15%
can be multiple or bilateral - unsual features
have cystic spaces, distincitive epithelium, lymphoid tissue, complete capusle
tx by excision
salivary gland carcinomas
how common
2 most common types
sites
15% of all salivary neoplasms
adenoid cystic carcinoma
mucoepidermoid
**minor salivary glands **
mucoepidemoid carcinomas
3-5%
minor glands
have 2 cell types
* squmous - epidermoid
* glandular - glandular
unpredictable behaviour and spread
adenoid cystic carcinoma
slow growing, painless, can ulcerate - pain
varied patterns
* cribiform - swiss cheese
* tubular
* solid
local spread - blood and nerves
difficult to tx - close to vital structures and recurrence; poor long term prognosis
trigeminal neuralgia symptoms
*(Associated with MS and Brain Tumour) - MRI needed esp young *
severe sudden onset pain (paroxysmal),
* electric shock
* lasts for a few seconds,
* may be associated with lacrimation;
* Trigger spots in 1/3 of pts.
follows unilateral side of trigeminal nerve branch(es), Very rarely bilateral.
trigemenial neuralgia casues
3
- idiopathic
- classical - vascular compression of CNV (MRI)
- secondary - MS; space occupying lesion
- others - skull base defomity, CT disease, atreriovenous malformation
aetiology of trigeminal neuralgia
damage or irritation to nerve
* CNV ischaemia, distoration of myelin sheath so interrupt or altered electrical conductivitvity
invesigation for trigeminal neuraligia
rule out odonogenic source of pain
MRI - assess focal demyelination on peripheral nerve and/or abberant intra craniall artery
FBC - carbmazepine has blood side effects so will need baseline
TN ref flags
3
young pt (>40years)
sensory deficit in facial region - hearling loss
other cranial nerve lesions
ALWAYS TEST CRANIAL NERVES
ALL PTS NOW GET MRI
management of TN
medications
* 1st line: carbmazepine/oxcarbazepine/lamotrigine
* 2nd line: gabapentin/ pregablin/phenytoin
surgery
* only if pt not managing on medications (side effects too much)
* younger pt - will need to be on drugs for long time
surgical otpions for TN
**microvascular decompression **
destructive central procedures
sterotactic radiosurgery
destructive peripheral nerectomies
medication for TN
should be responsive to carbmazepine (if tolerated)
* alter dosing regime to maximise efficacy with minimial side effects
* pain diary helpful
carbazepine side effects
Blood dyscrasias
* Thrombocytopenia
* Neutropenia
* Pancytopenia
Electrolyte imbalances (hyponatreamia) – careful if pt on diuretic, PPI (omeprazole)
Neurological deficits
* Paraesthaesia
* Vestibular problems
Liver toxicity
Skin reactions (including potentially life threatening)
cluster headache
attack
* restless, agitated - diff from migraine
* rapid onset and cessation of pain
* mainly oribital and temporal pain
* sharp throbbing
* 1-6 per day
bout
* attacks cluster into bouts with periods of remission
* attack circadian rhythm
abortive= sumatriptan; prevntative=topiramate
paroxysmal hemicrania
10% can be precipitated by bending or rotating head
80% chronic, 20% episodic
sharp throbbing
duration 2-30mins
2-40attacks per day (no circadian rhythm)
absolute response to indomethacin (prophylaxis)
alt med - COXII inhibiotrs, topiramate
