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Oral Medicine and Diagnosis > Vesiculobullous and Ulcerative Lesions Part 2 > Flashcards

Vesiculobullous and Ulcerative Lesions Part 2 Flashcards

1
Q

what is the etiology of benign mucous membrane pemphigoid

A
  • autoimmune; trigger unknown
  • autoantibodies directed against basement membrane zone antigens causes ulceration
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2
Q

what is the clinical presentation for BMMP

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
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3
Q

what is the 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
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4
Q

what is the dx for BMMP

A
  • biopsy
  • direct immunofluorescent examination
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5
Q

what is the DDX for BMMP

A
  • pemphigus vulgaris
  • erythema multiforme
  • erosive lichen planus
  • lupus erythematosus
  • epidermolysis bullosa acquisita
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6
Q

what are the microscopic findings for BMMP

A
  • subepithelial cleft formation
  • linear pattern IgG and complement 3 along basement membrane zone; less commonly IgA
  • direct immunofluorescence examination positive in 80% of cases
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7
Q

what is the treatment for mucous membrane pemphigoid

A
  • topical corticosteroids
  • systemic prednisone, azathrioprine or cyclophosphamide
  • tetracycline/niacinamide
    -dapsone
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8
Q

what is the prognosis for MMP

A
  • morbidity related to mucosal scarring (oropharyngeal, nasopharyngeal, laryngeal, ocular, genital)
  • managment often difficult due to variable response to corticosteroids
  • management often requires multiple specialists working in concert
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9
Q

what is the etiology for pemphigus vulgaris

A
  • an autoimmune disease where antibodies are directed towards 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
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10
Q

what is the clinical presentation for pemphigus vulgaris

A
  • over 50% of cases develop oral lesions as the initial manifestation
  • oral lesions develop in 70% of cases
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11
Q

what is the clinical presenation of pemphigus vulgaris

A
  • painful shallow irregular ulcers with friable adjacent mucosa
  • nonkeratinized sites (buccal, floor, ventral tongue) often are initial sites affected
  • positive nikolsky sign
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12
Q

in pemphigus vulgaris there are autoantibodies against:

A

intracellular bridges

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13
Q

what are the microscopic findings in pemphigus vulgaris

A
  • separation or clefting or 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
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14
Q

what is the diagnosis for pemphigus vulgaris

A
  • clinical appearance
  • mucosal manifestations
  • direct/indirect immunofluorescent studies
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15
Q

what is the differential diagnosis for pemphigus vulgaris

A
  • mucous membrane pemphigoid
  • erythema multiforme
  • erosive lichen planus
  • drug reaction
  • paraneoplastic pemphigus
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16
Q

what is the treatment for pemphigus vulgaris

A
  • systemic immunosuppression
  • prednisone, azathioprine, mycophenolate mofetil, cyclophosphamide
  • plasmapheresis plus immunosuppresson
  • IV Ig for some recalcitrant cases
17
Q

what is the oral management for pemphigus vulgaris

A
  • periodontal disease aggravates the condition
  • forming a relationship for maintenance and observation with a periodontist is prudent management
  • restorative treatment aggravates the condition
18
Q

what is the prognosis for pemphigus vulgaris

A
  • guarded
  • approximately a 5% mortality rate secondary to long term systemic corticosteroid related complications
19
Q

what is the etiology for lupus

A
  • an autoimmune/immunologically mediated condition
  • antibodies demonstrable against an array of cytoplasmic and nuclear antigens
  • most often occurs in women
20
Q

what are the 3 forms of lupus

A
  • chronic cutaneous (CCLE) or discoid (DLE)
  • subacute cutaneous (SCLE)
  • systemic (SLE)
21
Q

what is the clinical presentation for lupus

A
  • black females have highest incidence
  • predominates in women 40 years and older
  • 80% of patients have concurrent cutaneous findings
  • 30-40% of SLE patients have oral mucosal findings
  • oral mucsoal lesions may appear lichenoid, keratotic, and erosive
  • labial vermillion with crusted, exfoliative, erythematous, and keratotic appearance
  • oral findings are most common in CCLE or DLE
22
Q

what are the topical treatments for lupus erythematosus

A
  • flocinide gel/cream 0.05% 60g; apply after meals and at bedtime
  • tacrolimus (protopic) ointment 0.1% 30g; apply after meals 3 times daily, do not ear or drink for 30 minutes
  • intralesional therapy: triamcinolone acetonide 5-10mg/mL; inject 1-3mL per session with sessions at 3-4 week intervals
23
Q

what is the prognosis for lupus

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
24
Q

what is the etiology of erythema multiforme

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, barbituates
  • another trigger may be radiation therapy
25
Q

what is the clinical presentation for erythema multiforme

A
  • acute onset of multiple, painful shallwo 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
26
Q

what do the lesions look like in erythema multiforme

A
  • target or iris skin lesions may be noted over extremities
  • genital and ocular lesions may occur
  • usually self limiting; 2-4 week course
  • recurrence is common
27
Q

what is the dx for erythema multiforme

A
  • appearance - lip crusting
  • rapid onset
  • multiple site involvement in one half of cases
  • biopsy results often helpful but not always diagnostic
28
Q

what is the ddx for erythema multiforme

A
  • viral infection in particular acute herpetic gingivostomatitis
  • erythema multiforme rarely affects the gingiva
  • pemphigus vulgaris
  • major aphthous ulcers
  • erosive lichen planus
  • mucous membrane pemphigoid
29
Q

what is the treatment for erythema multiforme

A
  • mild (minor) form: symptomatic/supprotive 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
30
Q

what is the prognosis for erythema multiforme

A
  • generally excellent
  • recurrences common
31
Q

what is the etiology for stevens johnson syndrome

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
32
Q

what is one type of clinical presentation of stevens johnson syndrome

A
  • labial vermillion and anteiror 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
33
Q

what is the second type of clinical presentation for SJS

A
  • posterior oral cavity and oropharyngeal involvement leads to odynophagia, sialorrhea, drooling
  • eye involvement may occur
  • genital involvement may occur
  • cutaneous involvement may become bullous
  • iris or target lesions are characteristic on skin
34
Q

what is the dx for SJS

A
  • usually made on clinical grounds
  • histopathology is not diagnostic
35
Q

what is the DDX for SJS

A
  • pemphigus vulgaris
  • paraneoplastic pemphigus
  • mucous membrane pemphigoid
  • bullous pemphigoid
  • acute herpetic gingivostomatitis
  • stomatitis medicamentosa
36
Q

what is the treatment for SJS

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 0 acyclovir, famiciclovir
  • may require admission to hospital burn unit
37
Q

what is the prognosis for SJS

A
  • good, self limiting usually
  • recurrences not uncommon
38
Q
A

Oral Medicine and Diagnosis (5 decks)

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