Diseases of the Oral Mucosa and Skin II Flashcards
Lichen planus
(3)
Common, chronic disease that affects skin and oral mucosa
Immune mediated mucocutaneous disorder
Medications may cause similar appearance: lichenoid mucositis
Lichen planus
Clinical features:
MC in
Skin lesions:
Often affect
middle-aged female adults
purple, pruritic, polygonal, papules (4-P’s)
flexor surfaces of extremities
Lichen planus
Clinical features:
Reticular type: most common
(5)
Involves buccal mucosa bilaterally
Interlacing white lines – Wickham striae
Wax and wane
Post-inflammatory melanosis
Usually asymptomatic
Lichen planus
Clinical features:
Erosive type:
(4)
Atrophic, erythematous areas with central ulceration
Patients often symptomatic
Periphery bordered by fine, white radiating striae
Atrophy and ulceration confined to gingiva: desquamative gingivitis
Lichen planus
Diagnosis:
(2)
Clinical, histopathology, direct immunofluorescence
10% Formalin vs Michels solution
Lichen planus
Treatment:
Reticular:
Erosive:
usually asymptomatic, no tx needed
topical corticosteroids
Erythema multiforme
(3)
Ulcerative mucocutaneous condition of uncertain etiology
Likely an immune mediated process
50% of cases: precipitating cause – infections (ie: herpes simplex),
medications (infrequently)
Erythema multiforme
Clinical features:
Often observed in
symptoms
appearance
May appear as
young adults (20s and 30s)
Prodromal symptoms: Fever, malaise, headache, cough
Slightly elevated, round, dusky-red patches on skin
concentric circular erythematous rings – target lesion
Erythema multiforme
Clinical features:
most frequently involved mucosal site
(3) may be affected
Oral lesions:
(5)
Oral cavity
Ocular, genitourinary, respiratory mucosa
shallow erosions or ulcerations with irregular borders
Lips, labial mucosa, buccal mucosa, tongue, FOM, soft palate
Hemorrhagic crusting of the vermilion zone of lips
Erythema multiforme
Clinical features:
Erythema multiforme minor:
milder cases
Skin lesions and 1 mucosal site (usually oral)
Erythema multiforme
Clinical features:
Erythema multiforme major:
more severe
Widespread skin lesions and 2 or more mucosal sites
Severe ocular involvement: scarring (symblepharon formation)
Erythema multiforme
Treatment:
(2)
Usually self-limiting (2-6 weeks)
Systemic or topical corticosteroids
Stevens – Johnson syndrome
and Toxic epidermal necrolysis
SJS: —% skin and mucosal involvement
TEN: —% skin and mucosal involvement
Severe blistering diseases triggered by drug exposure
<10
>30
Stevens – Johnson syndrome
and Toxic epidermal necrolysis
Clinical features:
SJS: age
TEN: age
Initially present with
After a few days,
May have — changes as well
usually seen in younger patients
usually patients above 60 years
flu-like symptoms
cutaneous lesions appear on trunk
mucosal
After a few days, cutaneous lesions appear on trunk
(2)
Erythematous macules
Sloughing of the skin, flaccid bullae
Stevens – Johnson syndrome
and Toxic epidermal necrolysis
Treatment:
(3)
Identify, immediately discontinue offending drug
Management in burn unit of hospital
Mortality rate: SJS – 1-5% , TEN – 25-30%
Pemphigus vulgaris
(3)
Autoimmune disease
Immune attack on desmosomes – intra-epithelial split
1-5 cases per million people
Pemphigus vulgaris
Clinical features:
— lesions often first sign of disease, and most difficult to treat
Avg diagnosis age: — years
appearance
Affect any
Skin lesions:
Ocular lesions:
Oral
50
superficial, ragged erosions and ulcerations
oral mucosal location
Desquamative gingivitis
flaccid vesicles and bullae that rupture quickly
conjunctivitis
Pemphigus vulgaris
Clinical features:
(3)
Lesions persist and progress without treatment
Lesions are painful
Skin: positive Nikolsky sign: bulla appears with firm lateral pressure
Pemphigus vulgaris
Diagnosis:
(3)
Clinical, histopathology, direct immunofluorescence
10% Formalin vs Michels solution
Perilesional biopsy
Pemphigus vulgaris
Treatment:
Systemic corticosteroids, immunosuppressive drugs
Mucus membrane pemphigoid
Cicatricial pemphigoid
type
what
At least – more common compared to pemphigus
where
Autoimmune disease
Chronic, blistering, mucocutaneous disease
2x
Tissue-bound autoantibodies against components of basement membrane (ie:
hemidesmosomes)
Mucus membrane pemphigoid
Cicatricial pemphigoid
Clinical features:
— years of age
MC mucosal site:
mucosa
Oral lesions:
May rupture:
Lesions are —
50-60
oral cavity
Ocular, nasal, esophageal, laryngeal, vaginal
vesicles or bullae
large erosions and ulcerations
painful
Mucus membrane pemphigoid
Cicatricial pemphigoid
Clinical features:
May be observed in
Most significant complication:
May result in
any intraoral site
Desquamative gingivitis
ocular involvement – symblepharon formation
blindness
Mucus membrane pemphigoid
Cicatricial pemphigoid
Diagnosis:
(3)
Clinical, histopathology, direct immunofluorescence
10% Formalin vs Michels solution
Perilesional biopsy
Mucus membrane pemphigoid
Cicatricial pemphigoid
Treatment:
(3)
If only oral lesions present, may be controlled with topical corticosteroids
Patient should be referred to ophthalmologist
OHI measures for gingival lesions
Bullous pemphigoid
(3)
Autoimmune disease
Chronic, blistering, mucocutaneous disease
Tissue-bound autoantibodies against components of basement membrane (ie:
hemidesmosomes)
Bullous pemphigoid
Clinical features:
age
— is often an early symptom
— develop on skin – rupture after several days
Healing without —
75-80 years
Pruritis
Bullae
scarring
Systemic sclerosis
Scleroderma
(3)
May be immune-mediated condition
Dense collagen deposited throughout the tissue
Most organs of the body affected
Systemic sclerosis
Clinical features:
gender
Mainly observed in —
Often first noticed by
Skin develops —
Surface is usually —
Females: 2-3x more common
adults
cutaneous changes
diffuse, hard texture
smooth
Systemic sclerosis
Clinical features:
Involvement of facial skin:
— develops with perioral involvement
Tongue becomes —, — may develop
— may be present
Nasal ala becomes
Resorption of
smooth, taut, mask-like appearance
Microstomia
stiff, dysphagia
Xerostomia
atrophied – pinched appearance
Raynaud phenomenon
terminal phalanges → shortened clawlike fingers
Raynaud phenomenon:
vasoconstrictive event triggered by exposure to cold or stress
– often 1st sign of disease (fingers and toes)
Systemic sclerosis
Clinical features:
Involvement of other organs:
May eventually lead to
(3)
fibrosis of lungs, heart, GI tract
organ failure
Pulmonary fibrosis → pulmonary hypertension → heart failure
Systemic sclerosis
Radiographic features:
(2)
Widening of the PDL
Resorption of posterior mandibular ramus, condyle, coronoid process
Systemic sclerosis
Treatment: (2)
prognosis is poor
Systemic medications: penicillamine
CREST syndrome
Limited scleroderma
Calcinosis cutis, Raynaud phenomenon, Esophageal dysfunction, Sclerodactyly,
Teliangiectasia
CREST syndrome
Limited scleroderma
Clinical features:
MC gender, age
Calcinosis cutis:
Raynaud phenomenon:
Esophageal dysfunction:
Sclerodactyly:
Telangiectasia:
female, 6th – 7th decade
movable, subcutaneous nodules
severe vasospasm in fingers/toes
abnormal collagen deposition
finger becomes stiff, skin – smooth, shiny appearance
superficial dilated capillaries
Crohn’s disease
what
where
factor implicated
what may precede GI lesions
Inflammatory bowel disease, immune related
Anywhere in GI tract – mouth to anus
Genetic factor implicated
Oral lesions may precede GI lesions
Crohn’s disease
Clinical features:
MC Dx in – decade
symptoms (4)
Weight loss and malnutrition may develop →
Oral:
2nd
Abdominal cramping, pain, nausea, diarrhea
anemia, decreased growth
diffuse, nodular swelling, ulcers
Oral: diffuse, nodular swelling, ulcers
(2)
Cobblestone appearance
Erythematous macules and plaques
Crohn’s disease
Treatment:
(2)
Oral lesions typically clear with GI treatment
Sulfasalazine, antibiotics, corticosteroids
