white lesions part 2 (PMD) Flashcards
3 types of potentially malignant disorders
1) leukoplakia
2) oral lichen planus
3) lichenoid reactions
characteristics of leukoplakia
- what it looks like
- female/male
- cause
- predisposing factors
- is a white plaque that cannot be characterised clinically/ pathologically as another disease
- male predomincance, >40 yo, increase with age
- is uncommon, but the most common premalignant lesion
- unknown cause
- predisposing factors are the 6S:
sunlight, sex, syphilis, smoking, spirits (alcohol), spices (betel nut)
same factors as SCC and erythroplakia
6 types of clinical presentation of leukoplakia
1) early/ mild/ thin
2) nodular/ granular
3) homogenous/ thick
4) speckled/ erythroleukoplakia
5) verruciform
6) proliferative verrucous
what does early/ mild leukoplakia look like
- grey/ white plaque
- flat to slightly elevated
- soft with sharply demarcated borders
- may be translucent, fissured, wrinkled
clinical presentation of nodular/ granular leukoplakia
increase surface irregularities
clinical presentation of homogenous/ thick leukoplakia
- distinctly white plaque
- thickened/ leathery
- deepened fissures
clinical presentation of speckled/ erythroleukoplakia
- white plaque with scattered patches of redness
- epithelial cells so immature and atrophic that they cant produce keratin
clinical presentation of verruciform
sharp/ blunt wart-like projections
clinical presentation of proliferative verrucous
- multiple, slowly spreading, keratotic plaques
- rough surface projections
- exhibit persistent growth, eventually become exophytic and verrucous (wart-like)
location of leukoplakia
- lip vermillion, buccal mucosa and gingiva ( more common)
- lip vermillion, tongue, floor of mouth (accounts for >90% of those that show dysplasia/ carcinoma)
how to diagnose leukoplakia
clinical + histo (must take biopsy) + elimination of other lesions that appear as white plaque
histopatho findings of leukoplakia
- hyperkeratosis and ____
- variable number of ____ cells in subjacent _____
- keratin layer will have ____
- no/ got dysplasia?
- may have acanthosis
- chronic inflammatory cells, in aubjacent CT
- hyperorthokeratosis/ hyperparakeratosis or both
- may have dysplasia
management of leukoplakia that exhibit moderate dysplasia or worse
- complete removal
- recurrence rate 10-35%
mx of leukoplakia with no/minimal dysplasia
- mx should be guided by lesion size and response to tobacco cessation
- may diminish in size after smoking cessation
ddx of leukoplakia
white lesions:
- leukoedema
- BARK, frictional keratosis (linea alba, morsicato buccarum)
- nicotinic stomatitis, smokeless tobacco lesions
- OLP, lichenoid reactions
- pseudomembranous candidiasis
- OHL
not white lesions:
- syphilis (secondary mucous patches)
- squamous papilloma, condyloma acuminatum
what layers of epithelium are affected and what histo is observed in MILD epithelial dysplasia in leukoplakia
- basal and parabasal layers
- nuclear hypochromatism and slight pleomorphism
what layers of epithelium are affected and what histo is observed in MODERATE epithelial dysplasia in leukoplakia
- basal layer to mid portion of spinous layer
- nuclear hypochromatism and pleomorphism
- cellular crowding
what layers of epithelium are affected and what histo is observed in SEVERE epithelial dysplasia in leukoplakia
- basal layer to a level above midpoint of epithelium
- marked nuclear hyPER chromatism and pleomorphism
- scattered mitotic figures
- atypical cells involve most of epithelial thickness
what layers of epithelium are affected and what histo is observed in carcinoma in situ epithelial dysplasia in leukoplakia
whole thickness of epithelium
what is the cause of oral lichen planus
chronic t cell mediated disorder of stratified squamous epithelium (SSE), unknown cause
which demographic is more affected by OLP
middle aged adults, females
predisposing factors for OLP
drugs, restorative materials, microbes (hep C), systemic disorders, stress
pathogenesis of OLP
- antigen specific cd8+ cytotoxic t cells trigger keratinocyte apoptosis, destroy the basal keratinocytes above basement membrane
- mast cell granulation and MMP activation -> prolongs antiinflam reaction
7 forms of OLP
PAPERBD
papular: raised
atrophic: red, thin
plaque: white, flat
erosive: break in epithelium
reticular: striated
bullous: bubble appearance (less common)
desquamative gingivitis: red, painful, involve free gingi margin to mucogingival fold
histopatho findings for OLP
- varying degree of ___ and ___ on surface epithelium
- thickness of ___ layer varies
- ___, ____ rete ridges
- degeneration of ___ cell layer of epithelium
- degenerating ___ (Civatte bodies) between epithelium and ___
- intense, band like infiltrate of predominantly ____ in lamina propria
- got/ no dysplasia?
- varying degree of orthokeratosis and parakeratosis
- thickness of spinous layer
- pointed, saw toothed rete ridges
- degen of basal cell layer
- degenerating keratinocytes, between epithelium and CT
- infiltrate of predominantly t lymphocytes
- no dysplasia
forms and characteristics of erosive LP
AEBD forms:
- atrophic
- erythematous
- bullous (only if erosive component is severe and there is epithelial separation from the underlying CT)
- desquamative gingivitis (if the atrophy and ulceration is confined to gingiva mucosa)
characteristics:
- got central ulceration of varying degrees
- periphery bordered by fine, white radiating striae
2 types of OLP
1) erosive LP (AEBD forms)
2) reticular LP (PPR forms)
forms and characteristics of reticular LP
PPR: papules, keratotic plaques on tongue, reticular (striated)
characteristics:
- lace like network, striated pattern of slightly raised grey white lines (wickham striae)
- usually asymptomatic
symptoms of erosive LP
- erythematous and desquamative gingiva
- ulceration
- bleeding and irritation with tooth brushing
- oral pain and soreness, worse with acidic and spicy food
- sensitivity to hot, acidic, spicy food
- altered/ blunted taste sensation (if the tongue is affected)
location of OLP
- bilateral, mostly symmetrical
- posterior buccal mucosa > dorsal and lateral border of tongue > gingiva and alveolar ridge > lower lip
- floor of mouth, palate, upper lip (uncommon)
- skin, genital mucosa, scalp, nails (uncommon)
what are the 3 key histo points impt for the dx of OLP
- degeneration of basal cell layer of epithelium
- intense, band like infiltrate of predom t lymphocytes in lamina propria
- no dysplaisa
comparing leukoplakia and OLP
leukoplakia: single, well demarcated and non striated
OLP: bilateral, diffuse, striated
ddx of OLP
lichenoid reactions (have identical clinical and histo findings)
3 types of therapy that can be done under management of OLP
1) Symptomatic therapy
2) adjunctive therapy
3) maintenance therapy
symptomatic therapy for OLP
- control inflammation, decrease pain with minimal side effects
- change erosive OLP to non erosive
- 1st line: topical corticosteroids
- 2nd line: systemic corticosteroids for severe/ recalcitrant lesions resistant to topical. OR topical calcineurin inhibitors to block activation and prolif of t lymphocytes
example of topical calcineurin inhibitor
tacrolimus
adjunctive therapy for OLP
- control candida using topical anti fungals eg nystatin, miconazole
- maintain good OH
- manage salivary gland hypofunction if present
maintenance therapy for OLP
- low potency topical corticosteroids
- long term follow up
ddx for OLP
lichenoid reactions
what are lichenoid reactions
antigen fixation in epithelial cells causing these cells to be destroyed by immune system
these lesions resemble OLP clinically and histologically but have identifiable aetiology
4 types of lichenoid reactions that we learn
1) oral lichenoid drug reaction/ eruption
2) oral lichenoid contact lesions
3) oral lichenoid lesions of GVHD
4) systemic lupus erythematous
what are some drugs causing OLDR (oral lichenoid drug rxn)
methyldopa, anti malarias, NSAIDs, diuretics, ACE inhibitors, B blockers
what is the clinical presentation of OLDR
- unilateral lesions of reticular striae
- erosive lesions
- e/o lesions
location of OLDR in mouth
- palate
- labial mucosa
- floor of mouth
how do we dx OLDR
- need to establish when the lesion onset and when the offending drug was used
- see whether there is resolution of symptoms upon withdrawal of the agent
what are the histopatho findings of OLDR
- variable, non diagnostic
- lymphocytic infiltrate is mixed, more diffuse. this extends deeper into lamina propria, got perivascular distribution
mx for OLDR?
1) substitute drug after consulting physician
2) decrease dose of offending drug
3) topical corticosteroids (+/- anti fungals)
do these in order
ddx of OLDR and oral lichenoid contact lesions
OLDR: erosive OLP
OLCL: reticular OLP
where are oral lichenoid contact lesions found?
adjacent to dental materials
possible materials are Ni, composite, gic
usually buccal mucosa, ventral and lateral borders of tongue
clinical presentation of oral lichenoid contact lesions
- white or erythematous
- peripheral striae
histopatho findings of oral lichenoid contact lesions and oral lichenoid lesions of GVHD
- similar to OLP aka varying degree of ortho and parakeratosis on surface epithelium. pointed saw toothed rete ridges, degen of basal cell layer of epithelium, infiltrate of predom t lymphocytes in lamina propria
- lymphocytic infiltrated mixed
how do oral lichenoid lesions of GVHD come about
- hx of bone marrow transplant
- immunocompetent t cells from donor (graft) attack tissue in immunocompromised host (recipient)
- increased risk of developing solid tumours (eg SCC)
clinical presentation of oral lichenoid lesions of GVHD
- fine, reticular network of white striae
- may have atrophy of mucosa
- burning sensation of oral mucosa
where will oral lichenoid lesions of GVHD be located in mouth
- buccal and labial mucosa
- tongue
mx of oral lichenoid lesions of GVHD
- systemic therapy since it is a multi organ disease
1) give high dose systemic corticosteroids
2) supplement w cyclosporin, tacrolimus - topical corticosteroids (+/- anti fungals)
- long term follow up
ddx of oral lichenoid lesions of GVHD
reticular OLP
which are the lichenoid reactions that have ddx of reticular OLP and which have ddx of erosive OLP
reticular OLP:
1) oral lichenoid contact lesions
2) oral lichenoid lesions of GVHD
erosive OLP:
1) OLDR
2) SLE
clinical presentation of SLE
- central atrophic area with radiating white striae
- erythematous lesions on palate
- slit like gingival ulcerations
location of SLE in oral cavity
- palate (most common, 80%)
- buccal mucosa, lips, gingiva
vs OLP on palate is uncomon
how to dx SLE
must be by histo
histopatho findings of SLE
similar to OLP
may have deep perivascular distribution