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oral medicine and diagnosis > vesiculobollous and ulcerative lesions > Flashcards

vesiculobollous and ulcerative lesions Flashcards

1
Q

Lichen Planus general info
* Occurs in what decades
* mean age?
* Rare in what age group?
* % incidence;% with oral lesions have concomitant skin lesions
* % (cutaneous incidence); % also have oral lesions
* predominate demo?

A
  • Occurs in fourth to eighth decades
  • mean age in 5th decade
  • Rare in children
  • 3 to 4% incidence; 25% with oral lesions have concomitant skin
    lesions)
  • 0.5 to 1% (cutaneous incidence); 50% also have oral lesions
  • White females (60%)
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2
Q

distribution of LP

A
  • Bilateral and often quasi-symmetric
    distribution
  • Oral site frequency:
    1. buccal mucosa
    2. tongue
    3. gingiva
    4. lips
  • Skin sites: forearm, shin, scalp, genitalia
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3
Q

LP pathophys

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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4
Q

LP etiology
meds?
vax?
allergens?

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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5
Q

contributary factors to LP

A

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

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6
Q

Erosive LP clinical presentation

A

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

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7
Q

LP progression of symptoms

A

● asymptomatic
● itching
● episodic pain
● severe discomfort.

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8
Q

clinical forms of LP

A

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

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9
Q

reticular LP

A

● lacy
● striated
● “Wickham” striae

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10
Q
A

reticular LP

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11
Q

Erosive Lichen Planus locations

A

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

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12
Q

erosive LP presentation

A

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

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13
Q

Erosive LP symptoms

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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14
Q
A

bullous LP

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15
Q

Bullous Lichen Planus app

A

Small broken bullae/ulcers near white keratotic striae.

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16
Q

Differential Diagnosis for LP

A

lichenoid dysplasia
contact stomatitis
lichenoid reaction.

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17
Q

Treatment Goals LP

A

There is no cure, therefore;
Reduce length and severity of symptoms
Resolve oral mucosal lesions
Reduce risk of malignant degeneration to squamous cell carcinoma

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18
Q

Treatment Issues LP

A

Maintain good oral hygiene because meticulous oral hygiene reduces symptom severity

Oral hygiene is difficult to accomplish during active disease

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19
Q

Treatment options for LP (rx)

A

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

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20
Q

tx regimens LP

A

gel better than cream, less soluble

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21
Q

steroid carriers

A

Need to border mold the
impressions so tray extends
to mucobuccal folds for rx delivery

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22
Q

Intra-lesion steroid injections for LP

A

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

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23
Q

systemic roids for LP

A
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24
Q

antiviral tx for LP

A

Hydroxychloroquine (Plaquenil)
- relieve inflammation, swelling, stiffness, and joint pain

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25
Q

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
Treatment

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26
Q

Calcineurin inhibitors
used for?
forms?
what side effects when used systemically?

A

used for LP
pimecrolimus cream or tacrolimus ointment
Psychotic side effects when used systemically

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27
Q

untx risks of LP

A

Malignant potential Risk
– 0.1 – 0.2%
Erosive and ulcerative conditions have the greatest risk

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28
Q

Aphthous Stomatitis types

A
  1. Minor
  2. Major
  3. Herpetiform
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29
Q

Aphthous Stomatitis etiology
* viral or other infectious agent?
* probably represents?
* Triggers include?
* Human leukocyte antigen (HLA) subtype susceptibility?

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)
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30
Q

aphthous stomatitis membrane alterations

A

Alterations in mucosal membrane barrier permeability may be a factor because of co-morbidity associations with:
HIV/AIDS
bone marrow suppression
Neutropenia
gluten sensitivity
Crohn’s disease
ulcerative colitis
food allergy
Behçet disease
dietary deficiencies: iron, Zn, vitamin B12 (folate)

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31
Q

Aphthous
Stomatitis clinical description of ulcer

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

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32
Q
A

aphthous stomatitis

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33
Q

Aphthous Minor:
commonality?
* number?
* size?
* shape?
* healing time?

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

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34
Q
A

aphthous minor

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35
Q

aphthous major:
* size?
* number?
* depth?
*edges?
* length?
* Often heal with?

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
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36
Q
A

aphthous major

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37
Q

Herpetiform Aphthous Stomatitis

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
38
Q
A

herpetiform aphthous stomatitis

39
Q

Aphthous Stomatitis diagnosis
* Usually has diagnostic?
* History?
* family history?

A
  • Usually has diagnostic clinical appearance of focal, well- defined ulcers involving non- keratinized mucosa
  • History helpful; a recurrentprocess
  • Positive family history
40
Q

aphthous stomatitis dif dx

A
  • Traumatic ulcer
  • Chancre
  • Recurrent intraoral herpes simplex (HSV-1) stomatitis
  • Cyclic neutropenia
41
Q

Aphthous Stomatitis - Treatment
1. what may be adequate?
2. what, if present, should be addressed?
3. what oral rinses may be helpful?
4. what is most rational- most consistently effective? forms of this?
5. Other helpful agents?
6. Colchicine?
7. Thalidomide?

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
    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
  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
42
Q

Recurrent Aphthous Stomatitis
Recur as? more common recurrent form?
* In AIDS patients, lesions are typically?

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
43
Q

Benign Mucous Membrane Pemphigoid (BMMP)
Etiology

A
  • Autoimmune; trigger unknown
  • Autoantibodies directed against basement membrane zone antigens causes ulceration
44
Q

Benign Mucous Membrane Pemphigoid (BMMP)
Clinical Presentation
* intraoral sites?
* Usually in what age?
* gender?
* Ocular lesions noted in how many cases?
* scarring tendency?

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)
45
Q
A

Benign mucus membrane pemphigoid

46
Q

Nikolsky Sign

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
47
Q

Benign Mucous Membrane Pemphigoid
(BMMP)
Diagnosis

A
  • Biopsy
  • Direct immunofluorescent
    examination
48
Q

BMMP dif dx

A
  • Pemphigus vulgaris
  • Erythema multiforme
  • Erosive lichen planus
  • Lupus erythematosus
  • Epidermolysis bullosa acquisita
49
Q

BMMP microscope

A
  • Subepithelial cleft formation
  • Linear pattern IgG and complement C3 along basement membrane zone; less commonly IgA
  • Direct immunofluorescence examination positive in 80% of cases
50
Q

Mucous Membrane Pemphigoid Treatment
* Topical?
* Systemic?
* Abx?

A
  • Topical corticosteroids
  • Systemic prednisone, azathioprine, or cyclophosphamide
  • Tetracycline/niacinamide
  • Dapsone
51
Q

MMP prognosis?
Morbidity related to?
* Management often difficult due to?
* Management often requires?

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)

52
Q
A

Benign Mucous Membrane Pemphigoid
Cicatrixal Pemphigoid

53
Q

Cicatrixal Pemphigoids?

A

Recently ruptured bulla with epithelial cover still attached, likley to form scar in ocular, laryngeal, nasopharyngeal, and oropharyngeal tissues (Cicatricial Pemphigoid)

54
Q

is this symptomatic?

pt with BMMP

A

Massive, relatively painless sloughing of buccal mucosa, Cicatricial Pemphigoid

55
Q

Benign Mucous Membrane Pemphigoid
Gingival Variant

A

can also be localized to the gingiva

56
Q

other areas affected by BMMP

A

Eye, Mouth, Genitalia, Sometimes Skin

57
Q

Pemphigus Vulgaris
Etiologies

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
58
Q

Pemphigus Vulgaris:
* Over % of cases develop oral lesions as the initial
manifestation?
* Oral lesions develop in % of cases?

A
  • Over 50% of cases develop oral lesions as the initial
    manifestation
  • Oral lesions develop in 70% of cases
59
Q

app? initial sites? sign?

Pemphigus Vulgaris Clinical Presentation

A
  • Painful, shallow irregular ulcers with friable adjacent mucosa
  • Nonkeratinized sites (buccal, floor, ventral tongue) often are initial sites affected
    • Nikolsky sign
60
Q

Pemphigus Vulgaris Microscopic Findings

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

61
Q

Pemphigus Vulgaris
Diagnosis accomplished with?

A
  • Clinical appearance
  • Mucosal manifestations
  • Direct/indirect immunofluorescent studies
62
Q

PV dif dx

A
  • Mucous membrane (cicatricial)
    pemphigoid
  • Erythema multiforme
  • Erosive lichen planus
  • Drug reaction
  • Paraneoplastic pemphigus
63
Q

Pemphigus Vulgaris Treatment
* Systemic plan?
* options for this?
* Plasmapheresis?
* some recalcitrant cases may need?

A
  • Systemic immunosuppression
  • Prednisone, azathioprine, mycophenolate mofetil,
    cyclophosphamide
  • Plasmapheresis plus immunosuppression
  • IV Ig for some recalcitrant cases
64
Q

perio dx? restorative tx?

Pemphigus Vulgaris
Oral Management

A
  • Periodontal disease aggravates the condition
  • forming a relationship for maintenance and observation with a periodontist is prudent management
  • Restorative treatment aggravates the condition
65
Q

what can mortality be related to?

Pemphigus Vulgaris
Prognosis

A
  • Guarded
  • Approximately a 5% mortality rate secondary to long-term systemic corticosteroid–related complication
66
Q

Pemphigus Vulgaris Ab’s

A

Autoantibodies Against Intracellular Bridges

67
Q

Lupus Erythematosus Etiology

A
  • An autoimmune/immunologically mediated condition
  • Antibodies demonstrable against an array of cytoplasmic and nuclear antigens
  • Most often occurs in women
68
Q

Lupus Erythematosus
Three forms :

A
  1. Chronic cutaneous (CCLE) or
    discoid (DLE)
  2. Subacute cutaneous (SCLE)
  3. Systemic (SLE)
69
Q

Lupus Erythematosus Clinical Presentation
* demo with highest incidence
* Predominates in women >?
* 80% of patients have what other finding?
* % of SLE patients with oral mucosal findings?
* Oral mucosal lesions may appear as?
* Labial vermilion?
* Oral findings are most common in which forms?

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.
70
Q
A

lupus erythematosus

71
Q

pt also has malar rash

A

lupus erythematosus

72
Q

Lupus Erythematosus
Topical Treatments

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
73
Q

dif forms?

Lupus Erythematosus
Prognosis

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.
74
Q

Erythema Multiforme Etiologies:
* mediated by reactive process? possibly related to?

    • Many cases preceded by infection with?; less often with?
    • drugs?
    • Another trigger may be what therapy?
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.
75
Q

Erythema Multiforme Clinical Presentation
* onset/app?
* Early mucosal lesions are?
* May affect what surfaces? how? most commonly affected region and app?
severe form known as?

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

76
Q

acute onset, what is likely?

A

erythema multiforme

77
Q

EM demo

A

Predilection for young adults;
20-40 years

78
Q
A

erythema multiforme

79
Q

Erythema Multiforme systemic Clinical Presentation:
* lesions noted over extremities?
* Genital and ocular lesions?
* time frame?
* Recurrence?

A
  • Target or iris skin lesions may be noted over extremities.
  • Genital and ocular lesions may occur.
  • Usually self-limiting; 2- to 4-week course
  • Recurrence is commo
80
Q

Erythema Multiforme Diagnosis:
* Appearance?
* onset?
* how many sites involved?
* Biopsy?

A
  • Appearance (note lip crusting)
  • Rapid onset
  • Multiple site involvement in one-half of cases
  • Biopsy results often helpful, but not always diagnostic
81
Q

EM dif dx

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
82
Q

Erythema Multiforme Treatment:
* Mild (minor) form:
* * Severe (major) form:

    • If evidence of an antecedent viral infection or trigger exists, what can help?
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.
83
Q

EM prognosis

A
  • Generally excellent
  • Recurrences common
84
Q

Stevens-Johnson Syndrome Etiology:
* A complex mucocutaneous disease
affecting?
* Most common trigger:
* Infection with what other spp can also may
serve as a trigger?
* Medication trigger?
* Sometimes referred to as ?

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”
85
Q

Stevens-Johnson Syndrome Clinical Presentation 1
* areas usually affected initially?
* lesion progression?
* later appears?
* Pseudomembrane involved?

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
86
Q

Stevens-Johnson Syndrome Clinical Presentation 2:
* Posterior oral cavity and oropharyngeal involvement leads to?
* Eyes?
* Genitals?
* Cutaneous involvement?
* lesions characteristic on skin?

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
87
Q

Stevens-Johnson Syndrome
Diagnosis
* Usually made on?
* Histopathology?

A
  • Usually made on clinical grounds
  • Histopathology is not diagnostic
88
Q

SJS dif dx

A
  • Pemphigus vulgaris
  • Paraneoplastic pemphigus
  • Mucous membrane (cicatricial)
    pemphigoid
  • Bullous pemphigoid
  • Acute herpetic gingivostomatitis
  • Stomatitis medicamentosa
89
Q

Stevens-Johnson Syndrome
Treatment:
* symptomatic measures?
* oral rinses?
* use of what is controversial?
* Recurrent, virally associated cases may be reduced in frequency with use of?
* May require admission to?

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
90
Q

SJS prognosis

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

oral medicine and diagnosis (6 decks)

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