benign lesions of the oral mucosa Flashcards
are most congenital/hereditary or acquired?
some congenital/hereditary but majority are acquired
epithelial origin lesions
papilloma
drug-induced gingival overgrowth
lamina propria origins
traumatic fibroma pyogenic granuloma peripheral GC granuloma mucocele lipoma haemangioma
papilloma aetiology
neoformation epithelial origin
HPV
clinical papilloma
hairy like elongated lesion single/multiple white/pinkish pedunculated/sessile no malignant potential
tx papilloma
surgical - may recur
another name for traumatic fibroma
fibroepithelial polyp
location of traumatic fibroma
usually buccal mucosa, lips, tongue
NOT gingiva
traumatic fibroma aetiology
accidental biting
chronic irritation
trauma/infection
traumatic fibroma clinical presentation
dome-shaped soft same colour as surrounding mucosa, can be keratinised sessile/pedunculated can be ulcerated
what is a traumatic fibroma called if on gingivae?
epulis
traumatic fibroma tx if excessive dimension
surgically remove
traumatic fibroma histology
fibrous tissue
covered by keratinised SSE
- buccal mucosa NK: paler cells (store glycogen)
- to withstand trauma
- atrophic - thinner than normal epithelium
collagen fibres, fibroblasts, a few chronic inflammatory cells
- relatively acellular CT
drugs responsible for drug-induced gingival overgrowth
anticonvulsants - phenytoin
immunosuppressants - cyclosporin
Ca channel blockers - nifedipine, amlodipine
clinical presentation drug-induced gingival overgrowth
enlargement 1-3m of taking drug entire U and L gingiva more severe anterior regions starts from ID papilla may cover a portion or entire tooth crown
drug-induced gingival overgrowth consequences
may prevent OH
painful eating
disfigurement
impair QOL
drug-induced gingival overgrowth tx
liase w physician: discontinuation of drug and switch to another
professional OH and CHX rinse
gingivectomy
if med not stopped may recur
pyogenic granuloma aetiology
benign, vascular, reactive?
aetiology unknown
- seems constant insults may lead to rapid proliferation of capillaries w a friable and lobulated aspect
hormonal factors - associated with pregnancy
clinical presentation pyogenic granuloma
begins small red papule
then red pedunculated exophytic lesion
surface often friable and ulcers - bleeding
often gingival margin (vascular epulis) and tongue
pyogenic granuloma consequences
no malignant potential but complications - ulceration, bleeding, secondary infections
pyogenic granuloma tx
surgical (but may recur)
also to stop angiomatous proliferation or to rule out chancre, carcinoma or kaposi-sarcoma
peripheral giant cell granuloma/GC epulis aetiology
usually described as reaction to chronic local factors
- supra/subgingival dental biofilm
- ill fitting Rxs
- dentures
- associated to implants
unknown aetiology - seems to come from PDL, or periosteum, or persistence of cells from PDL after tooth ext
peripheral giant cell granuloma/GC epulis clinical
younger pts anterior exophytic smooth red/purple firm/elastic consistency freq asymptomatic except if surface ulcerated
peripheral giant cell granuloma/GC epulis radiographic
resorption alv bone
widening PDL space
rarely RR
peripheral giant cell granuloma/GC epulis histology
MN GCs with background of GT
mononuclear stromal cells and extravased rbcs, v cellular
sharply demarcated but no fibrous capsule surrounding
hyperlastic SSE - parakeratinised
red cell areas - haemorrhage
- haemosidrin - brown
GCs might be macrophages joined together
peripheral giant cell granuloma/GC epulis tx
conservative excision with PD therapy
but high chance of recurrence
exclude systemic disease
- raised PTH
- low vit D in diet
- malabsorption
- renal disease
CGCG (bony)
uncommon
found only in tooth bearing regions of jaws
most common in mandible 20-30yrs
may mimic malignant neoplasm
can erode through cortical bone - domed purplish mucosal swelling
may have haemosidrin due to new and old haemorrhages (v vascular)
mucocele aetiology
lesion caused by disruption of salivary flow from minor salivary glands origin
types of mucoceles
extravasation
- collection of saliva in CT following trauma to ducts
retention
- accumulation of saliva within ductal system due to obstruction of the salivary ducts
ranula
- from major salivary gland origin, occur on FOM
mucocele clinical
soft neoformations
usually L lip and buccal mucosa
colour from normal mucosa to light blue/white
tend to be larger and smaller periodically
- may want to wait 2-3m to see if it gets larger. Bursts and recurs
mucocele tx
surgical removal inc underlying minor salivary gland
mucocele histology
wall of GT lined by compact layer of macrophages saliva in lumen foam cells - some macrophages break off into cyst to try and absorb saliva - become large foam cells cystic cavity
lipoma aetiology
uncertain
hereditary/endocrine/trauma/infections?
genetic, Gardner syndrome
lipoma definition
neoplasm from adipose tissue
lipoma clinical
submucosal mobile yellowish to pinkish soft to fibrous long-lasting swellings
covered by normal oral mucosa
as gets bigger may ulcerate
buccal mucosa and tongue most common
lipoma histology
adipose tissue
lipoma tx
usually none
but if painful/growing SR
recurrences uncommon
white sponge naevus aetiology
congenital/hereditary
thought to be due to mutations in genes responsible for making keratin and also shedding mucosa
white sponge naevus clinical
asymptomatic
affects NKSSE - buccal mucosa, ventral tongue, FOM, SP
white sponge naevus histology
normally don’t biopsy
parakeratosis with intracellular oedema in keratin layer
acanthosis
white sponge naevus tx
none
how oral mucosa reacts to trauma depends on:
irritation
time (how long and how many times)
person (genetics)
reactions may be in form of:
- inflammation
- keratosis
- ulceration
- fibrous tissue formation
- vesicles and bullae
- other types
epulis
any ST swelling on gingiva
parakeratinised
when keratin contains remains of nuclei
orthokeratinised
no nuclei remnants in keratin
haemangioma aetiology
benign, enlarged vascular tumour
develops due to abnormal proliferation of blood vessels
- endothelial cells
usually present at birth - developmental hamartoma
- tends to grow first 6m of life
- then shrinks as becomes fibrotic
blood present within vessels and is in continuation with circulation of rest of body
hamartoma composed of vascular tissue
haemangioma presentation
painless, smooth/lobulated, sessile/pedunculated soft mass
red/blue/purple
blanching effect - pressure causes disappearance, when released fill up slowly again
haemangioma histology classification
capillary: small capillaries lined by a single layer of endothelial cells supported in a CT stroma
cavernous: large, thin-walled vessels, or sinusoids lined by epithelial cells, separated by thin CT layer
haemangioma tx
usually none, can undergo spontaneous regression
small % - tx with surgery, laser, intralesional injection of fibrosing agent
herpes simplex/PHG
inflammation/formation of vesicles which easily rupture and can coalesce don't biopsy ballooning degeneration - operlant colour - large size - may fuse
fibrous epulis cause
reaction to trauma - form of chronic inflammation
- will recur if don’t address cause
fibrous epulis clinical
mainly fibrous tissue firm pink ST swelling keratinised areas of ulceration most common posterior gingivae
fibrous epulis histology
SSE - hyperplastic or ulcerated, parakeratinised
ulceration
- break in continuity of epithelium
- surface zone distinctly pink/yellow, base fibrin
- zone just beneath ulceration highly cellular and vascular (GT)
mass of GT
- 1st stage of healing
- capillaries, fibroblasts, macrophages, plasma cells, neutrophils, lymphocytes
LP - white
- papillae project upwards into epithelium
- rete pegs - epithelial, project downwards into LP
metaplastic bone formation
- reprogramming of mesenchymal SCs that are present -
produce bone
- reaction to chronic low grade irritation/trauma
- tissue may feel “gritty” when remove
- uniform pink staining areas
- less cellular
fibrous epulis tx
surgical removal
scaling
OHI
vascular epulis presentation
gingivae (if not on gingivae pyogenic granuloma - same)
lots of bv’s - bleeds lots
vascular epulis aetiology
thought to be exaggerated response of tissue to some sort of chronic trauma
pregnancy? - most commonly found - pregnancy epulis
- and changing OCP
- delay removal until after birth - becomes fibrotic and smaller so easier to remove
vascular epulis outcome
fairy simple to remove but may recur if inflammation/subgingival calculus isn’t txed
vascular epulis histology
base has epithelium (darkest bit) - remove base or recurrence likely - pedunculated/sessile no epithelium on surface - ulcerated - red (inflammation) and yellow (fibrin) surface - get fibrin from fibrinogen - part of clotting process after bleeding vascular loose CT - GT - neutrophils - lots of bv's - can bleed into GT - fibroblasts - macrophages - plasma cells
GC epulis/granuloma - ruling out underlying bone lesion
radiograph as look the same histologically as other GC lesions
- osteitis fibrosa cystica (brown tumour) in
hyperparathyroidism
- central GC granuloma: grows along jaw in AP direction,
causes erosion of alveolar bone, pops out and sits on
gingiva as GC epulis - esp if lesion keeps recurring
suspect this
- OFG
- TB
- sarcoidosis
- foreign body GC granuloma (e.g. suture or amalgam)
denture-induced hyperplasia
fibrous overgrowth
trauma from denture flange
if fix denture it may resolve but may need surgical removal
leaf fibroma
on hard palate (get squashed by denture)
papillary hyperplasia of palate
pseudo-epitheliomatous hyperplasia - GT, covered on surface by hyperplastic keratinised SSE - groups of epithelial cells
denture associated
what condition is haemangioma associated with?
Sturge-Weber syndrome
- can involve oral mucosa/alv bone
- can rarely affect brain meninges - epilepsy
- distribution of lesions corresponds to area innervated by branches of CN5 - don’t cross midline
hamartoma
tumour-like overgrowth of tissues which are normally found at the site
growth usually limited to a certain period, not lesions of continued growth - distinguishes from neoplasm
vascular malformation
same as haemangioma but appears later on (though present at birth)
- atrophy/trauma/calcification may make them visible
atrophy
thinning of the epithelium
- skin may appear dry and wrinkled
causes of atrophy
age
nutritional deficiency - iron, vit B12, folate
chronic sun exposure
inflammatory and neoplastic skin diseases
- cutaneous T cell lymphoma
- lupus erythematosus
long term use of potent topical CS
consequence of atrophy
predisposes to infection - protective fct down
histology of an ulcer
epithelium hyperplastic and keratinised
break in continuity of epithelium - ulcer
surface of ulcer - fibrin with inflammatory cells and necrotic tissue, yellow
base - GT moves up and new bv’s
deep to that zone of inflammatory cells - plasma cells
epithelium at margins
- comes to abrupt end
- atrophic and keratinised with inflammatory cells present in the epithelium
what do keratosis and hyperplasia in an ulcer suggest?
that there has been frictional irritation and therefore the chronic irritation at the point where the epithelium has broken down has exceeded the epithelial capacity to react
white edge to an ulcer
keratin - can occur when get trauma to a NK surface - forms keratin to try and protect itself - frictional keratosis
non-specific ulcer
no characteristic features to diagnose it as anything else
- not malignant
- can be aphthous, traumatic etc
types of oral mucosa
masticatory
gustatory (specialised)
lining - NK
types of ulceration
trauma ROU - RAS - infections - secondary to systemic disease carcinoma
env causes of ulceration
trauma allergy smoking infection stress
what often causes a papilloma?
HPV 6 and 11
histology of papilloma
hyperkeratotic surface papillary (finger-like) projections projections have fibrovascular CT cores SSE covers cores no dysplasia
condyloma acuminatum
wart
HPV 6, 11, 16 and 18
tongue and palate
condyloma acuminatum histology
acanthotic and sometimes hyperkeratotic epithelium with occasional koilocytosis
