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Oral Pathology > Developmental and Immune-mediated Mucocutaneous Diseases > Flashcards

Developmental and Immune-mediated Mucocutaneous Diseases Flashcards

1
Q

T/F. Ectodermal dysplasias is a group of inherited diseases in which three or more ectodermally derived structures do not develop normally or fail to develop.

A

False, Ectodermal dysplasias is a group of inherited diseases in which TWO or more ectodermally derived structures do not develop normally or fail to develop.

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2
Q

What areas are affected with ectodermal dysplasia?

A

skin, hair, nails, teeth, or sweat glands

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3
Q

In ____ E.D., there is heat intolerance due to reduced ___ glands.

A

hypohidrotic; sweat

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4
Q

What condition has patients who appear with fine, sparse blonde or light colored hair, eyebrows and eyelashes? How would you describe their teeth?

A

Hypohidrotic ED

oligodontia (lack of development of SIX or more teeth) with conical teeth.

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5
Q

How is ED managed?

A
  1. genetic counseling

2. prosthetic dental management (dentures, overdentures, fixed appliances, dental implants)

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6
Q

Patients misdiagnosed with ED may have what condition? If the patients mother undergoes sterilization unnecessarily, what are the odds of this problem affecting other offspring?

A

polygenetic oligodontia

1:100,000

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7
Q

White sponge nevus is an autosomal ___ condition known as “___” that is relatively ___(common/rare).

A

dominant; genodermatosis; rare

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8
Q

When is WSN first noticed?

A

at birth or in early childhood, sometimes noticed first in adolescence

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9
Q

WSN is due to a defect in the normal ___ of the oral mucosa.

A

keratinization

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10
Q

WSN is a ___ (symptomatic/asymptomatic), thick, white appearance of the ___ (buccal/lingual) mucosa ___ (unilaterally/bilaterally), but other oral sites may be affected as well.

A

asymptomatic; buccal; bilaterally

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11
Q

In addition to the buccal mucosa, what other mucosa are involved in WSN?

A

nasal, esophageal, larynegeal, anogenital

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12
Q

T/F. Biopsy is sometimes more diagnostic than an exfoliative cytology sample of WSN.

A

False, exfoliative cytology is more diagnostic than a biopsy.

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13
Q

What is seen on the biopsy sample of WSN?

A

parakeratosis with acanthosis (thickening of spinous layer)

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14
Q

What is pathognomonic or unique to WSN?

A

epithelial cells that often show perinuclear eosinophilic condensation of cytoplasm

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15
Q

T/F. WSN prognosis is poor and treatment varies depending on severity of the disease.

A

False, WSN prognosis is good and no treatment is necessary.

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16
Q

T/F. Peutz-Jeghers syndrome is relatively common and inherited as an autosomal recessive trait.

A

False, it is relatively RARE but well recognized condition that is usually inherited as an autosomal DOMINANT trait.

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17
Q

What percentage of PJS represents new mutations?

A

35%

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18
Q

In PJS, the ___ gene is affected – encodes for a ___/___ kinase.

A

SKT11; serine/threonine

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19
Q

PJS is usually noticed in ___ (childhood/adults) and characterized by ___-like lesions which develop on the hands, periorificial skin (mouth, nose, anus, genital region) and oral mucosa.

A

childhood; freckles

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20
Q

T/F. In PJS, polyps develop in the GI tract, especially in the duodenum.

A

False, polys usually develop in the jejunum and ileum

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21
Q

PJS can cause bowel obstruction due to ___ or “___” of a proximal segment into a distal segment.

A

intussusception; telescoping

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22
Q

T/F. When intussusception occurs in PJS, it may self correct but surgery is sometimes needed to prevent ischemic necrosis.

A

True.

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23
Q

T/F. Similarly to Garners syndrome, PJS polyps are also precancerous.

A

False, they are not precancerous.

GI polyps appear as benign hamartomatous growths of intestinal glandular epi

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24
Q

T/F. PJS patients have an increased susceptibility to cancer that is about 2 times greater than a control population.

A

False, PJS patients have an increased susceptibility to cancer that is about 18 times greater than a control population

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25
Q

How is PJS treated?

A
  1. genetic counseling

2. monitor for intussusception and for tumor development

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26
Q

Hereditary Hemorrhagic Telangiectasia is an uncommon autosomal ___ disorder that is estimated to have a frequency of about 1 in ___.

A

dominant; 10,000

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27
Q

HHT is due to a mutation in one of ___ different genes that play a role in blood vessel ___ integrity.

A

2; wall

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28
Q

Define telangiectasia.

A

small collection of dilated capillaries.

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29
Q

What is often an initial clue of HHT?

A

spontaneous epistaxis

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30
Q

What is noted on the oropharyngeal and nasal mucosae of HHT?

A

numerous 1-2mm red papules that blanch with diascopy

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31
Q

Where are HHT lesions most commonly found?

A
  1. vermilion zone of lips
  2. tongue
  3. buccal mucosa
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32
Q

Where is telangiectasias seen?

A

hands and feet, GI mucosa, GU mucosa, and conjunctival mucosa

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33
Q

Arteriovenous fistulas may affect the lungs (___% of patients), liver (___%), or brain (___-___%).

A

30; 30; 10-20

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34
Q

How can a diagnosis of HHT be made?

A

if a patient has 3 of 4 features:

  • recurrent spontaneous epistaxis
  • telangiectasias of mucosa and skin
  • AV malformation involving the lung, liver, or brain
  • family history
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35
Q

T/F. Histologically, a collection of thin-walled blood vessels in the superficial connective tissue is seen in HHT.

A

True.

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36
Q

In addition to genetic counseling, what treatment is given for HHT patients with mild, moderate and severe forms of the disease?

A

mild - no treatment
moderate - selective cryotheraphy or electrocautery of bothersome lesions
severe - septal dermoplasty to prevent epistaxis

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37
Q

What is sometime necessary in HHT patients with significant GI involvement and blood loss?

A

iron replacement or transfusion

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38
Q

T/F. HHT patients with AV fistula involving the brain do not need prophylactic antibiotics before dental procedures.

A

False, prophylactic antibiotics before dental procedures that cause bacteremia have been suggested due to the 1% prevalence of brain abscess in these patients.

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39
Q

T/F. HHT prognosis is generally poor with 1-2% mortality in patients who develop a brain abscess and 10% mortality in those with blood loss complications.

A

False, HHT prognosis is generally GOOD, with 1-2% mortality in those with BLOOD LOSS complications and 10% in those with BRAIN ABSCESS.

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40
Q

What is the etiology of Pemphigus Vulgaris?

A

autoimmune

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41
Q

In PV, autoantibodies destroy ___.

A

desmosomes, which bond epithelial cells together. Antibodies inhibit adherence and a split develops in the epithelium

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42
Q

T/F. PV is a rare disorder seen in males in their 20s. PV is usually fatal if not treated.

A

Statement 1 is false. Statement 2 is true.

1: PV is rare and has no sex predilection and is seen in individuals around 50 yo.
2: it is usually fatal if not treated due to severe infection, loss of fluids/electrolytes, and malnutrition due to mouth pain

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43
Q

What percentage of PV presents with mouth lesions?

A

greater than 50%

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44
Q

Patients with PV have superficial, ___ erosion and ___ found on ___ oral mucosal surface.

A

ragged; ulcerations; any

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45
Q

PV has ___ ___ on skin and intact oral blisters are ___ (commonly/rarely) seen.

A

flaccid bullae; rarely

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46
Q

What term is used when inducing a bulla by applying firm, lateral pressure to normal appearing skin?

A

+ Nikolsky sign

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47
Q

What is being referenced with the phrase “first to show last to go”?

A

the oral lesion seen in PV

In other words, the oral lesions are the initial manifestation of the disease and the most difficult to resolve with treatment.

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48
Q

What is a technique that uses fluorescent-labeled antibodies to detect specific targets?

A

immunofluorescence

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49
Q

___ immunofluorescence is used to detect autoantibodies bound to the patient’s tissues. ___ immunofluorescence is used to detect autoantibodies circulating in the blood.

A

Direct; Indirect

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50
Q

T/F. Normal tissue adjacent to ulceration or erosion should not be sampled for DIF. Both DIF and IFF immunofluorescence studies will be negative for pemphigus vulgaris

A

Both statements are false.

1: Normal tissue adjacent to ulceration or erosion SHOULD be sampled for DIF.
2: Both DIF and IFF immunofluorescence studies will be POSTIVE for pemphigus vulgaris

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51
Q

In PV, autoantibodies bind ___ components, specifically desmoglein ___ & ___.

A

desmosomal; 1; 3

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52
Q

When sampling tissue in PV, where should the sample be taken from?

A

the periphery not the ulcerated center.

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53
Q

In PV, microscopically, ___ clefting ___ (above/below) the basal layer (i.e. ___ (within/outside) the epithelium).

A

intraepithelial; above; within

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54
Q

In PV, what is the process where there is breakdown of the spinous layer and cells fall apart?

A

acantholysis

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55
Q

T/F. In PV, patients are treated with topical steroid because systemic corticosteroids have little affect.

A

False, they are treated with systemic corticosteroids, often with azathioprine or other steroid-sparing agents. topical steroids have little effect

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56
Q

What percentage of PV patients died prior to corticosteriod therapy? What is the mortality rate today?

A

60-90%

5-10%, usually due to complications of therapy

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57
Q

What is another term for Mucous Membrane Pemphigoid?

A

cicatricial (“scarring”) pemphigoid

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58
Q

How does MMP clinically resemble PV? How common is MMP to PV?

A

due to blister formation

At least 2x more common than PV

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59
Q

T/F. MMP is usually seen in females around the age of 50-60.

A

True

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60
Q

MMP can affect ___ mucosal surface (occasionally skin) but scarring is usually seen with ___ (___) and cutaneous lesions.

A

any; conjunctival (symblepharon)

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61
Q

With MMP, ___ blisters will be seen intraorally but ___ scarring is rare.

A

intact; oral

62
Q

What is a descriptive term denoting erythema, desquamation, and ulceration appearance that can be seen in several disorders?

A

desquamative gingivitis

63
Q

MMP often presents as ___ ___. It is not uncommon that gingival tissues are the ___ (first, last, only) affected site.

A

desquamative gingivitis; only

64
Q

What is the most significant aspect of MMP?

A

ocular involvement

65
Q

In MMP, ___ obstructs the orifices of glands that produce the ___ film, resulting in a dry eye. Dryness leads to ___ of the ___ epithelium, leading to blindness.

A

scarring; tear; keratinization; corneal

66
Q

When sampling the periphery of the MMP lesion, what must it include?

A

a generous portion of normal mucosa, as epithelium easily strips off

67
Q

In MMP, microscopic examination shows ___ cleft formation – separation of the epithelium from the connective tissue at the ___.

A

SUBepithelial; BMZ (basement membrane)

68
Q

In MMP, submit normal mucosa, ___-___cm away from areas of ulceration/erythema. Tissue should be submitted in both ___ solution and ___ (ideally).

A

0.5 - 1.0 cm; Michel’s; formalin

69
Q

What is seen in MMP at the BMZ (basement membrane)?

A

linear deposition of immunoreactants

70
Q

MMP is postive for ___ (DIF/IFF) and negative for ___ (DIF/IFF) because only ___-___% of patients will have circulating autoantibodies.

A

DIF; IFF; 5-25%

71
Q

T/F. MMP treatment depends on the extent of involvement. Oral lesions alone are treated with topical steroids, tetracycline/niacinamide or dapsone.

A

Both statements are true.

72
Q

How often should MMP patients receive dental prophylaxis?

A

frequently q 3-4 mos.

73
Q

In MMP, if there is ___ involvement, systemic immunosuppressive therapy is indicated.

A

ocular

74
Q

T/F. MMP is fatal and is difficult to control. Blindness results in patients with untreated ocular disease.

A

The first statement is false the second is true.

1: MMP is rarely fatal and the condition can usually be controlled.

75
Q

T/F. MMP undergoes spontaneous resolution.

A

False, it RARELY undergoes spontaneous resolution

76
Q

Bullous pemphigoid usually affects ___(younger/older) populations.

A

older

77
Q

T/F. In BP, oral involvement is primarily seen and cutaneous lesions are uncommon.

A

False, Cutaneous lesions are seen primarily - oral involvement seems to be uncommon (but has been reported to be from 8-39%).

78
Q

With BP, ___ is common initial complaint, followed by cutaneous blisters.

A

pruritus

79
Q

What does BP and MMP have in common?

A

SUBepithelial cleft

80
Q

BP has a positive for which immunofluorescence test?

A

both DIF and IFF, with immunoreactants deposited at the BMZ

81
Q

Compare the treatment of BP and MMP.

A

management is similar to ciicatricial pemphigoid, but most BP cases resolve spontaneously in 1-2 yrs

82
Q

___ ___ has an acute onset and is a self-limiting (2-6 weeks) ulcerative disorder.

A

Erythema Multiforme

83
Q

EM is a ___-mediated disease seen in ___ (young/old) women (in more recent studies).

A

immune; young (20-30)

84
Q

Match the etiology of EM.

A. 25%
B. 50%

  1. medication-related (especially antibiotics and analgesics)
  2. preceding infection; viral (herpes) or bacterial (Mycoplasma pneumoniae)
  3. unknown
A
  1. A
  2. A
  3. B
85
Q

Describe the EM - minor and major spectrum of disease.

A

EM-minor: skin or mucosa only

EM-major: (Stevens-Johnson syndrome) at least two mucosal sites plus skin involvement

86
Q

What condition is seen with EM that has diffuse bullous involvment of skin and mucosa?

A

toxic epidermal necrolysis (Lyell’s disease)

87
Q

Clinically, EM patients have ___ crusting of lips, widespread oral ulcers with ___ margins and “___” lesions of skin.

A

hemorrhagic; ragged; target

88
Q

T/F. In EM, the gingiva and hard palate are common locations. The labial mucosa, buccal mucosa and tongue are usually spared.

A

Both statements are false. In EM, the labial mucosa, buccal mucosa and tongue are common locations. The gingiva and hard palate are usually spared.

89
Q

T/F. Light microscopic features are characteristic but not diagnostic in EM.

A

True.

90
Q

Histologically, EM has ___ destruction, ___ edema, mixed inflammatory infiltrate, and ___ inflammation.

A

keratinocyte; subepithelial; perivascular

91
Q

T/F. In EM, there is no useful immunologic patter. DIF is only used to rule out another immunobullous process.

A

Both statements are true.

92
Q

T/F. For mild cases of EM, supportive care and steroid syrup can help. For EM minor, corticosteroids are often given empirically because the patient will likely heal anyway.

A

Both statements are true

93
Q

How is EM with SJS treated?

A

if a toxic drug is identified, D/C the drug

94
Q

How is EM with TEN treated?

What should be avoided?

A

it is managed in the burn unit. IV pooled human immunoglobin.

Avoid corticosteroids

95
Q

EM is recurrent in ___% of cases and usually in the ___ and ___ (summer/autumn/winter/spring - pick 2)

A

20; autumn; spring

96
Q

In recurrent episodes of EM, seek to identify initiating factor - ___ or ___.

A

HSV (continuous retroviral therapy given); drugs

97
Q

The prognosis of EM is ___ for mild to moderate cases. EM major has a __-__% mortality rate and TEN has a ___% mortality rate.

A

good; 2-10; 34

98
Q

What is another term for erythema migrans?

A

benign migratory glossitis

geographic tongue

99
Q

What is a common (1-3% of pop) oral condition where patients report waxing and waning of lesions that heal then develop in a different area?

A

erythema migrans

100
Q

Erythema migrans is often seen with a ___ tongue and the lesions present on the ___ and ___ anterior 2/3s.

A

fissured; dorsal; lateral

101
Q

What term is used with erythema migrans develops on other non-keratinized mucosal surfaces?

A

ectopic geographic tongue

102
Q

Erythema migrans is described with multiple, well-demarcated zones of ___ surrounded at least partially by a slightly elevated yellow-white ___ or ___ border.

A

erythema; serpentine; scalloped

103
Q

Similar to psoriasis, EMigrans biopsies are usually diagnosed as “___ ___”.

A

psoriasiform mucositis

104
Q

EMigrans has ___ with extensive ___ formation in the superificial ___ layer that causes shearing off of the ___, with the remaining epithelium being much thinner, resulting in a ___ appearance.

A

parakeratosis; microabscess; spinous; parakeratin; red

105
Q

T/F. EMigrans has no treatment and some patient may complain of sensitivity to hot or spicy foods.

A

True.

106
Q

T/F. Cutanteous Lichen Planus is a chronic immune-mediated disorder that affects female adults aged 30 - 60.

A

True.

107
Q

CLP has ___ polygonal pruritic papules with ___ ___ that affects the ___ surfaces of wrist, ___ region and ___.

A

purple; Wickham’s striae; flexor; lumbar; shins

108
Q

What are the two forms of Oral Lichen Planus? Which is more common? Symptomatic?

A
  1. reticular lichen planus - most common

2. erosive lichen planus - most symptomatic

109
Q

T/F. Reticular LP has shallow ulcers, peripheral erythema and radiating white lines. Erosive LP has interlacing white lines.

A

Both statements are false.

Erosive LP has shallow ulcers, peripheral erythema and radiating white lines. Reticular LP has interlacing white lines.

110
Q

The dorsal tongue in Oral LP have appear as patchy ___ and ___.

A

keratosis; atrophy

111
Q

Microscopically, oral LP has ___, alternating ___ and thickening of the ___ layer with absent or pointed ___ ___, degeneration of the ___ cell layer and a band-like infiltrate of ___.

A

hyperkeratosis; atrophy; spinous; rete ridges; basal; lymphocytes

112
Q

T/F. Oral LP is not a clinical diagnosis therefore clinical findings should be correlated with the microscopic findings.

A

False, Oral LP IS a clinical diagnosis therefore clinical findings should be correlated with the microscopic findings.

113
Q

What is also treated with Oral LP?

A

candidiasis

114
Q

How is reticular LP treated?

A

it requires no therapy, patients often notice a “roughness” of the buccal mucosa but it does not hurt.

115
Q

How is erosive LP treated?

A

with one of the stronger TOPICAL corticosteriods and systemic steroids are not needed

116
Q

T/F. Oral LP has a high potential to become malignant and therefore its prognosis is poor.

A

False. Oral LP has a good prognosis and there is no molecular evidence supporting malignant potential.

117
Q

___ ___ ___ is the most common of the significant immune-mediated systemic diseases.

A

Systemic Lupus Erythematosus

118
Q

What type of patient is typically found to have SLE?

A

women affected 8 to 10 times more than men
women of color
31 years

119
Q

Clinically how do patients with SLE present?

A

protean manifestations (fever, weight loss, arthritis, fatigue, general malaise)
malar “butterfly” rash that spares nasolabial folds
skin lesions flare with sun exposure

120
Q

Renal involvement is seen in ___-___% of SLE patients and it can lead to kidney failure. Cardiac involvement is common, particularly ___.

A

40-50%; pericarditis

121
Q

___% of SLE patients have sterile vegetations on heart valves (Libman-Sacks endocarditis).

A

50

122
Q

How often and where are oral lesions found in SLE?

How are they treated?

A

5-25%

palate, buccal mucosa or gingiva

They usually respond to topical corticosteroids.

123
Q

How is SLE diagnosed?

A

clinical, histopathologic, immunopathologic, and serologic findings

lichenoid pattern microscopically, perivascular inflammation

124
Q

T/F. The negative lupus band test shows deposition of a band of immunoreactants at the basement membrane zone of normal skin. It is not specific to SLE.

A

1st statement is false, 2nd is true

1: The POSITIVE lupus band test shows deposition of a band of immunoreactants at the basement membrane zone of normal skin.
2. some Lupus patients are negative for the lupus band test

125
Q

Serum studies show __-___ antibodies (ANAs) present in ___% of SLE patients. This is a ___-___ finding but can be used as a screening tool.

A

anti-nuclear; 95; non-specific

126
Q

___% of SLE patients are specifically directed to ___-___ ___, these are more specific.

A

70%; double-stranded DNA

127
Q

Treatment of SLE includes decreasing patients exposure to what? How is mild disease and significant cases treated?

A

UV light

non-steroidal anti-inflammatory or anti-malarial drugs and systemic corticosteroids (arthritis, pericarditis, nephritis, thromboyopenia)

128
Q

What is the prognosis, 5 and 15 year survival rate and most common cause of death for SLE?

A

prognosis is variable adn worse for men
5 year - 95%
15 year - 75%
death - renal failure

129
Q

What is another term for chronic cutatneous lupus?

A

discoid lupus

130
Q

T/F. Chronic cutaneous lupus is a different disease from SLE that almost exclusively affects the skin and mucosa. It waxes and wanes adn oral lesions resemble erosive LP.

A

Both statements are true.

131
Q

CCLupus has ___, erythematous patches on sun-exposed skin of the head and neck. Scarring and atrophy of these lesions with healing leads to a ___ problem.

A

scaly; cosmetic

132
Q

What is characteristic of CCLupus? What is seen microscopically?

A

skin lesions is usually characteristic

oral lesions show lichenoid mucositis and vasculitis

133
Q

T/F. Serologic studies of CCLupus are positive for anti-nuclear antibodies.

A

False, it is usually negative

134
Q

How is CCLupus treated?

A

avoiding excessive UV light exposure
topical corticosteroids
systemic malarial drug or low dose thalidomide

135
Q

CCLupus prognosis is ___ than SLE with approximately ___% transforming to SLE. Lesion are usually confined to skin and ___% eventually resolve after several years.

A

better; 5; 50

136
Q

What is a relatively rare condition that is characterized by inapporpriate deposition of dense collagen that affects 20 cases/million annually?

A

systemic sclerosis

137
Q

In SS, adult women are affected ___ times more than men.

A

3

138
Q

What condition describes discoloration of teh fingers and/or toes after exposure to changes in temperature or emotional events?

A

Raynaud’s phenomonon (not specific to SS)

139
Q

SS patients have ___-like deformity of fingers due to ___ deposition and ulceration of the fingertips. When the digit tips and bone can be destroyed it is called ___-___.

A

claw; collagen; acro-osteolysis

140
Q

SS has a diffus smooth, hard texture of skin termed “___” and has also been termed “___”.

A

hidebound; scleroderma

141
Q

T/F. In SS, pulmonary, renal, cardiac and GI fibrosis may be seen with pulmonary HTN. Heart failure is a common cause of death.

A

Both statements are true.

142
Q

SS patients have microstomia with pinched “___-___” appearance of mouth. Dysphagia occurs with ___ involvement.

A

purse-string; esophageal

143
Q

T/F. SS shows widened PDL and resorption of posterior ramus, condyle, coronoid process or chin in 10-20% with tooth resorption seen sometimes.

A

True.

144
Q

Histologically shows dense ___ deposition and serologic studies show autoantibodies directed against ___ (___).

A

collagen; Scl-70 (topoisomerase I)

145
Q

What is seen more with CREST syndrome?

A

anti-centromere antibodies

146
Q

How is SS treated?

A

no good definitive treatment

supportive care includes esophageal dilation, calcium channel blockers to ease Raynaud’s syndrome, ACE inhibitors to control HTN

problems with Oral hygiene and prosthese

147
Q

__-__% of SS survive ___ years after diagnosis.

A

30-50; 8

148
Q

CREST syndrome is a milder form of SS. What does it stand for?

A 
Calcinosis cutis
Raynaud's phenomenon
Esophageal dysfunction
Sclerodactyly
Telangiectasia
149
Q

What group does CREST occur in?

A

women, 6th to 7th decade of life

150
Q

What is the prognosis and 6 and 12 year survival rate for CREST syndrome?

A

better prognosis than SS
6 year - 80%
12 year - 50%

Oral Pathology (5 decks)

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