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Oral Medicine > Vesiculobullous and Ulcerative Lesions > Flashcards

Vesiculobullous and Ulcerative Lesions Flashcards

1
Q

Oral lichen planus vs cutaneous
more frequent?
more persistent/resistant?

A

Oral lichen planus (OLP) more frequently than
the cutaneous LP
OLP tends to be more persistent and more
resistant to treatment

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2
Q

LP
age
(3)

A
  • Occurs in fourth to eighth decades
  • mean age in 5th decade
  • Rare in children
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3
Q

LP
—% incidence; —% with oral lesions have concomitant skin
lesions)
* —% (cutaneous incidence); –% also have oral lesions
* White females (60%)

A

3 to 4, 25
0.5 to 1, 50

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4
Q

LP
of 362 cases
- Candidiasis –%
- BMS –%
- OLP –%

A

12
10
8

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5
Q

LP
distribution

A

Bilateral and often quasi-symmetric
distribution

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6
Q

LP
* Oral site frequency: (4)
* Skin sites: (4)

A
  1. buccal mucosa
  2. tongue
  3. gingiva
  4. lips

forearm, shin, scalp, genitalia

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7
Q

LP
Pathophysiology
(3)

A

not infectious
not hypersensitivity
autoimmune disease; T-lymphocytes
attack Langerhan cells in epithelium of
affected areas
Causes chronic inflammatory lesions
with varying episodes of intensity

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8
Q

LP
Etiology
(5)

A

● NSAID’s (ibuprofen and naproxen)
● Various medications for heart disease,
hypertension (hydrochorthiazide, etc.) ,
rheumatoid arthritis
* Hepatitis C infection and other types of
liver disease
* Vaccines - Hepatitis B, various flu vaccines,
effect of the COVID vaccine uncertain
* Food allergens, dental materials or other
substances

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9
Q

LP
Etiology Instigating Factors
(2)

A

Co-morbidities are contributary
- Diabetes
Vices are contributary
- EtOH, tobacco, etc.

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10
Q

LP
Clinical Presentation
(4)

A

● Erythematous
● Ulcerated
● Keratotic striations
● episodic pain to severe discomfort

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11
Q

LP
Clinical Symptoms
(4)

A

● asymptomatic
● itching
● episodic pain
● severe discomfort

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12
Q

LP
Clinical Types
(4)

A

Reticular -
Erosive –
Patch –
Bullous –

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13
Q

Reticular -
Erosive –
Patch –
Bullous –

A

Reticular - most common
Erosive – most painful
Patch – simulates dysplasia
Bullous – clinically similar to diseases of greater
morbidity

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14
Q

Reticular Lichen Planus
(3)

A

● lacy
● striated
● “Wickham” striae

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15
Q

Erosive Lichen Planus
(4)

A

Buccal and labial mucosa
tongue laterodorsum
Gingiva
Palate (???)

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16
Q

Erosive Lichen Planus
apperance (2)

A

Large, irregular atrophic erythematous patches
diffuse outlines
Progress to ulcerations, pseudomembranous cover

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17
Q

Erosive Lichen Planus
pain
symptoms
sympoms result in

A

Episodic pain to severe discomfort
Symptoms may persist weeks or longer
Symptoms result in weight loss, nutritional
deficiencies and depression

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18
Q

LP
Differential Diagnosis
(3)

A

lichenoid dysplasia
contact stomatitis
lichenoid reaction

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19
Q

LP
Treatment Goals
There is no cure, therefore;
(3)

A

Reduce length and severity of symptoms
Resolve oral mucosal lesions
Reduce risk of malignant degeneration to
squamous cell carcinoma

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20
Q

LP
Treatment Issues
Maintain good oral hygiene
because

A

meticulous oral hygiene reduces
symptom severity
Oral hygiene is difficult to accomplish
during active disease

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21
Q

LP
Treatment
(4)

A

Oral anesthetic rinse (1% Dyclonine solution)
Antibiotics
Antifungals (with steroid);
nystatin with triamcinolone
(Mycostatin II)
Corticosteroids

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22
Q

LP
Treatment Regimens
Topicals -

A

4-6 week course
- most popular; best success with steroid carriers

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23
Q

LP
Treatment Regimens
Mild –
(2)

A

cortisone 5% ointment
triamcinolone 0.1% ointment

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24
Q

LP
Treatment Regimens
Moderate –
(3)

A

cortisone 10% ointment
fluocinonide gel 0.05%
dexamethasone 0.05% ointment

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25
Q

LP
Treatment Regimens
Potent –
(2)

A

clobetasol 0.05% ointment/gel
halobetasol 0.05% ointment

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26
Q

Steroid Carriers vs. Bleaching Trays

A

need to border mold the
impressions so tray extends
to mucobuccal folds

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27
Q

LP
Treatment
Intra-lesion steroid injections
(2)

A

12 mg/week dexamethasone for 8 weeks
5 -10 mg/week triamcinolone PRN

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28
Q

LP
Treatment
Systemic steroids
Prednisone ~

A

2 – 3 weeks
loading dose 0.5 to 1 mg/kg/day (40 -80mg/qd)
- Need tapering down regimen

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29
Q

LP
Treatment
Methotrexate (antimetabolite)

A

10 to 20mg once weekly for 4- 12 weeks

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30
Q

LP
Other treatments
Hydroxychloroquine (Plaquenil)
(2)

A

-disease-modifying anti-rheumatic
drug (DMARD); anti-malarial
- relieve inflammation, swelling,
stiffness, and joint pain

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31
Q

LP
Other treatments
Thalidomide

A

Bad history when used in pregnancy for anxiety, morning
sickness, headache, etcc. (1950s);
Thalidomide babies had lack of appendage development (arms,
legs). Other aplasias - ears or malformed kidneys.
Contemporary use for inflammatory mucocutaneous diseases

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32
Q

LP
Other treatments
Calcineurin inhibitors
(3)

A

pimecrolimus cream
tacrolimus ointment
Psychotic side effects when used systemically

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33
Q

LP Untreated risks
Malignant potential Risk
– %
(2) conditions
have the greatest risk
Untreated risks

A

0.1 – 0.2
Erosive and ulcerative

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34
Q

Aphthous Stomatitis
Three Types

A
  1. Minor
  2. Major
  3. Herpetiform
35
Q

Aphthous Stomatitis
Affects 18 to 27% of the population;
prevalence is approximately –%

A

20

36
Q

Aphthous
Stomatitis
Etiology - unknown
(4)

A
  • no viral or other infectious agent
    identified
  • probably represents focal
    immunodysfunction but the specific
    mechanism is undetermined.
  • Triggers include increased stress/anxiety,
    hormonal changes, dietary factors,
    trauma, etc…)
  • Human leukocyte antigen (HLA) subtype
    susceptibility a factor in some cases (-
    B12, -B51, and others)
37
Q

Aphthous
Stomatitis
Alterations in mucosal membrane barrier
permeability may be a factor because of
co-morbidity associations with:

A

HIV/AIDS
bone marrow suppression
Neutropenia
gluten sensitivity
Crohn’s disease
ulcerative colitis
food allergy
Behçet disease
dietary deficiencies
iron
Zn
vitamin B12 (folate)

38
Q

Aphthous
Stomatitis
Clinical Description of Ulcers
(3)

A
  • Recurrent, self-limiting,
    painful ulcers
  • Usually restricted to
    nonkeratinized oral and
    pharyngeal mucosa (not
    hard palate or attached
    gingiva)
  • Well-demarcated ulcers
    with yellow fibrinous base
    and erythematous halo
39
Q

Aphthous Minor
(5)

A
  • most common subtype
  • Single but more often
    multiple
  • Less than 1 cm in diameter
  • Oval to round shape
  • Healing within 7 to 14 days
40
Q

Aphthous Major
(a.k.a. Sutton’s Disease)
(6)

A
  • 1 cm or greater in diameter
  • Single or less commonly several
  • Deep
  • To ragged edges with elevated edematous margin
  • May persist for several weeks to months
  • Often heal with scarring
41
Q

Herpetiform Aphthous Stomatitis
(7)

A
  • least common variant
  • Grouped superficial ulcers
    1-2 mm dia
  • crops of 10 to 100 lesions
  • lesions coalesce
  • In nonkeratinized and
    keratinized tissues
  • Healing within 7 to 14 days
  • No etiologic role for herpes
    simplex virus
42
Q

Aphthous
Stomatitis
Diagnosis
(3)

A
  • Usually has diagnostic clinical
    appearance of focal, well-
    defined ulcers involving non-
    keratinized mucosa
  • History helpful; a recurrent
    process
  • Positive family history
43
Q

Aphthous
Stomatitis
Differential Diagnosis
(4)

A
  • Traumatic ulcer
  • Chancre
  • Recurrent intraoral herpes
    simplex (HSV-1) stomatitis
  • Cyclic neutropenia
44
Q

Aphthous
Stomatitis
Treatment
(7)

A
  1. Symptomatic therapy may be adequate.
  2. Systemic causative factors, if present, should be
    addressed.
  3. Tetracycline-based oral rinses may be helpful.
  4. Corticosteroid therapy - most rational
    - most consistently effective
  5. Other immunomodulating drugs may be helpful
    (dapsone, hydroxychloroquine, topical tacrolimus,
    amelexanox).
  6. Colchicine (0.6–1.2 mg/d) is sometimes beneficial.
  7. Thalidomide treatment has shown efficacy in
    clinical trials
45
Q
  1. Corticosteroid therapy - most rational
    - most consistently effective
    (3)
A

a. Topical corticosteroids as gels, creams, or
ointment 4 to 6 times/d to early lesions
b. Intralesional corticosteroid injections
c. Short-duration systemic corticosteroids (low to
moderate doses

46
Q

Recurrent Aphthous Stomatitis
(4)

A
  • Recur as minor or major variants
    Minor is more common recurrent form
  • Minor; episodic: 1– 4 episodes/year;
    few lesions, usually minor or herpetiform)
  • Major; almost continuous ulcerations; disabling,
    large, or severe lesions)
  • In AIDS patients, lesions are typically more severe
    and may occur on any oral surface
47
Q

Benign Mucous Membrane Pemphigoid
(BMMP)
Etiology
(2)

A
  • Autoimmune; trigger
    unknown
  • Autoantibodies directed
    against basement
    membrane zone antigens
    causes ulceration
48
Q

Benign Mucous Membrane Pemphigoid
(BMMP)
Clinical Presentation

A
  • Vesicles and bullae followed by
    ulceration
  • Multiple intraoral sites
    (occasionally gingiva only)
  • Usually in older adults
  • 2:1 female predilection
  • Ocular lesions noted in one-third
    of cases
  • scarring tendency in ocular,
    laryngeal, nasopharyngeal, and
    oropharyngeal tissues (Cicatricial
    Pemphigoid)
49
Q

Nikolsky Sign
(2)

A
  • Epithelial splitting
  • application of firm lateral shearing force on uninvolved skin or mucosa can produce a
    surface slough or induce vesicle formation

Broken bullae leave open, painful ulcerations

50
Q

Benign Mucous Membrane Pemphigoid
(BMMP)
Diagnosis
(2)

A
  • Biopsy
  • Direct immunofluorescent
    examination
51
Q

Benign Mucous Membrane Pemphigoid
(BMMP)
Differential Diagnosis
(5)

A
  • Pemphigus vulgaris
  • Erythema multiforme
  • Erosive lichen planus
  • Lupus erythematosus
  • Epidermolysis bullosa acquisita
52
Q

Benign Mucous Membrane Pemphigoid
(BMMP)
Microscopic Findings
(3)

A
  • Subepithelial cleft formation
  • Linear pattern IgG and complement 3 (C3) along
    basement membrane zone; less commonly IgA
  • Direct immunofluorescence examination positive in
    80% of cases
53
Q

Mucous Membrane Pemphigoid
Treatment
(4)

A
  • Topical corticosteroids
  • Systemic prednisone, azathioprine, or
    cyclophosphamide
  • Tetracycline/niacinamide
  • Dapsone
54
Q

Mucous Membrane Pemphigoid
Prognosis
(3)

A
  • Morbidity related to mucosal scarring
    (oropharyngeal,
    nasopharyngeal, laryngeal, ocular, genital)
  • Management often difficult due to variable
    response to
    corticosteroids
  • Management often requires multiple specialists
    working in concert (dental, dermatology,
    ophthalmology, otolaryngology)
55
Q

Pemphigus Vulgaris
Etiology
(2)

A
  • An autoimmune disease where
    antibodies are directed toward the
    desmosome-related proteins of the
    epithelial intercellular bridges
    (desmoglein 3 or desmoglein 1)
  • A drug-induced form exists with less
    specificity in terms of immunologic
    features, clinical presentation, and
    histopathology
56
Q

Pemphigus Vulgaris
Clinical Presentation
(2)

A
  • Over 50% of cases develop
    oral lesions as the initial
    manifestation
  • Oral lesions develop in 70% of
    cases
57
Q

Pemphigus Vulgaris
Clinical Presentation
(3)

A
  • Painful, shallow irregular
    ulcers with friable adjacent
    mucosa
  • Nonkeratinized sites (buccal,
    floor, ventral tongue) often are
    initial sites affected
    • Nikolsky sign
58
Q

Pemphigus Vulgaris
Microscopic Findings
(8)

A
  • Separation or clefting of suprabasal from basal layer of
    epithelium
  • Intact basal layer of surface epithelium
  • Vesicle forms at site of epithelial split
  • Direct immunofluorescence examination positive in all cases
  • IgG localization to intercellular spaces of epithelium
  • C3 localization to intercellular spaces in 80% of cases
  • IgA localization to intercellular spaces in 30% of cases
  • General correlation with severity of clinical disease
59
Q

Pemphigus Vulgaris
Diagnosis
(3)

A
  • Clinical appearance
  • Mucosal manifestations
  • Direct/indirect
    immunofluorescent studies
60
Q

Pemphigus Vulgaris
Differential Diagnosis
(5)

A
  • Mucous membrane (cicatricial)
    pemphigoid
  • Erythema multiforme
  • Erosive lichen planus
  • Drug reaction
  • Paraneoplastic pemphigus
61
Q

Pemphigus Vulgaris
Treatment
(4)

A
  • Systemic immunosuppression
  • Prednisone, azathioprine,
    mycophenolate mofetil,
    cyclophosphamide
  • Plasmapheresis plus
    immunosuppression
  • IV Ig for some recalcitrant cases
62
Q

Pemphigus Vulgaris
Oral Management
(3)

A
  • Periodontal disease aggravates the
    condition
  • forming a relationship for
    maintenance and observation with a
    periodontist is prudent management
  • Restorative treatment aggravates the
    condition
63
Q

Pemphigus Vulgaris
Prognosis
(2)

A
  • Guarded
  • Approximately a 5% mortality rate
    secondary to long-term systemic
    corticosteroid–related complications
64
Q

Benign Mucous Membrane Pemphigoid
Cicatrixal Pemphigoid
(3)

A

Eyes and genitalia are
often involved.
Blister is beneath the
epithelium.
Antibodies attack the
basement membrane

65
Q

Pemphigus Vulgaris
(3)

A

Primarily a skin disorder.
Blister is within the
epithelium.
Antibodies attack the
intercellular bridges.

66
Q

Lupus Erythematosus
Etiology
(3)

A
  • An autoimmune-
    /immunologically mediated
    condition
  • Antibodies demonstrable
    against an array of cytoplasmic
    and nuclear antigens
  • Most often occurs in women
67
Q

Lupus Erythematosus
Three forms :

A
  1. Chronic cutaneous (CCLE) or
    discoid (DLE)
  2. Subacute cutaneous (SCLE)
  3. Systemic (SLE)
68
Q

Lupus Erythematosus
Clinical Presentation
(7)

A
  • Black females have highest incidence
  • Predominates in women > 40 years
  • 80% of patients have concurrent
    cutaneous findings
  • 30 to 40% of SLE patients have oral
    mucosal findings
  • Oral mucosal lesions may appear
    lichenoid, keratotic, and erosive.
  • Labial vermilion with crusted,
    exfoliative, erythematous, and
    keratotic appearance
  • Oral findings are most common in
    CCLE or DLE.
69
Q

Lupus Erythematosus
Topical Treatments
(3)

A
  • Fluocinonide gel/cream 0.05% 60 g; apply after
    meals and at bedtime
  • Tacrolimus (Protopic) ointment 0.1% 30 g; apply
    after meals 3 times daily, do not eat or drink for 30
    min
  • Intralesional therapy: triamcinolone acetonide 5–
    10 mg/mL; inject 1–3 mL per session with sessions
    at 3–4 wk intervals
70
Q

Lupus Erythematosus
Prognosis
(3)

A
  • Good prognosis with CCLE or DLE form
  • Variable prognosis with SLE
  • SCLE has an intermediate prognosis between that of SLE and
    CCLE or DLE forms.
71
Q

Erythema
Multiforme
Etiology (4)

A

Immunologically mediated reactive
process, possibly related to
circulating immune complexes
* Many cases preceded by infection
with herpes simplex; less often with
Mycoplasma pneumoniae or other
organisms
* May be related to drug consumption,
including sulfonamides, other
antibiotics, analgesics,
phenolphthalein-containing
laxatives, barbiturates
* Another trigger may be radiation
therapy.

72
Q

Erythema
Multiforme
Clinical Presentation
(5)

A
  • Acute onset of multiple, painful,
    shallow ulcers and erosions with
    irregular margins
  • Early mucosal lesions are
    macular, erythematous, and
    occasionally bullous.
  • May affect oral mucosa and skin
    synchronously or
    metachronously
  • Lips most commonly affected
    with eroded, crusted, and
    hemorrhagic lesions
    (serosanguinous exudate)
    known as Stevens-Johnson
    syndrome when severe
  • Predilection for young adults;
    20-40 years
73
Q

Erythema
Multiforme
Target or iris skin lesions may be noted over —
* (2) lesions may occur.
* Usually self-limiting; – week course
* Recurrence is common

A

extremities.
Genital and ocular
2- to 4-

74
Q

Erythema
Multiforme
Diagnosis
(4)

A

Appearance (note lip crusting)
* Rapid onset
* Multiple site involvement in one-half of cases
* Biopsy results often helpful, but not always diagnostic

75
Q

Erythema
Multiforme
Differential Diagnosis
(4)

A
  • Viral infection, in particular, acute
    herpetic gingivostomatitis (Note:
    Erythema multiforme rarely
    affects the gingiva.)
  • Pemphigus vulgaris
  • Major aphthous ulcers
  • Erosive lichen planus
  • Mucous membrane (cicatricial)
    pemphigoid
76
Q

Erythema Multiforme
Treatment
(4)

A
  • Mild (minor) form: symptomatic/supportive treatment
    with adequate hydration, liquid diet, analgesics, topical
    corticosteroid agents
  • Severe (major) form: systemic corticosteroids, parenteral
    fluid replacement, antipyretics
  • If evidence of an antecedent viral infection or trigger
    exists, systemic antiviral drugs during the disease or as a
    prophylactic measure may help.
  • See “Therapeutics” section for details
77
Q

Erythema Multiforme
Prognosis
(2)

A
  • Generally excellent
  • Recurrences common
78
Q

Stevens-Johnson Syndrome
Etiology
(5)

A
  • A complex mucocutaneous disease
    affecting two or more mucosal sites
    simultaneously
  • Most common trigger: antecedent
    recurrent herpes simplex infection
  • Infection with Mycoplasma also may
    serve as a trigger.
  • Medications may serve as initiators
    in some cases.
  • Sometimes referred to as “erythema
    multiforme major”
79
Q

Stevens-Johnson Syndrome
Clinical Presentation 1
(4)

A
  • Labial vermilion and anterior portion of oral cavity usually
    affected initially
  • macular lesions erode, then slough, and ulcerate
  • later appear crusted and hemorrhagic.
  • Pseudomembrane; foul-smelling presentation as bacterial
    colonization supervenes
80
Q

Stevens-Johnson Syndrome
Clinical Presentation 2
(5)

A
  • Posterior oral cavity and
    oropharyngeal involvement
    leads to odynophagia,
    sialorrhea, drooling
  • Eye (conjunctival) involvement
    may occur.
  • Genital involvement may
    occur.
  • Cutaneous involvement may
    become bullous.
  • Iris or target lesions are
    characteristic on skin.
81
Q

Stevens-Johnson Syndrome
Diagnosis
(2)

A
  • Usually made on clinical
    grounds
  • Histopathology is not
    diagnostic.
82
Q

Stevens-Johnson Syndrome
Differential Diagnosis
(5)

A
  • Pemphigus vulgaris
  • Paraneoplastic pemphigus
  • Mucous membrane (cicatricial)
    pemphigoid * Bullous
    pemphigoid
  • Acute herpetic
    gingivostomatitis
  • Stomatitis medicamentosa
83
Q

Stevens-Johnson Syndrome
Treatment
(5)

A
  • Hydration and local symptomatic measures
  • Topical compounded oral rinses
  • Systemic corticosteroid use controversial
  • Recurrent, virally associated cases may be reduced in
    frequency with use of daily, low-dose antiviral
    prophylactic therapy (acyclovir, famciclovir, valacyclovir).
  • May require admission to hospital burn unit
84
Q

Stevens-Johnson Syndrome
Prognosis
(2)

A
  • Good; self-limiting usually
  • Recurrences not uncommon

Oral Medicine (13 decks)

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