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Oral Pathology > White Lesions > Flashcards

White Lesions Flashcards

1
Q

Reasons lesions may be white:

A
  1. Intracellular edema 2. Plaques 3. Reduced vascularity 4. Fungal colonies
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2
Q

White lesions that can be scraped off

A
  1. White coated tongue
  2. Pseudomembranous candidiasis
  3. Thermal burn
  4. Sloughing traumatic lesion
  5. Toothpase reaction
  6. Chemical burn
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3
Q

White lesions that can’t be scraped off:

A
  1. Heridirary conditions
  2. Reaction lesions
  3. Preneoplastic lesion
  4. Lesions due to EBV
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4
Q

Which herditary lesion is not a true one?

A

Leukoedema

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5
Q

Features of leukoedema

A
  • General opacification of buccal mucosa
  • Asymptomatic
  • BILATERAL
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6
Q

Why does leukoedema have a grayish-white color?

A

It’s more common in African-Americans

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7
Q

Common populations with leukoedema

A

Smokers and African Americans

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8
Q

Pathognomonic sign of leukoedema

A

Disappears when the mucosa is stretched

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9
Q

Histopathology of leukoedema

A

Epithelium: parakeratotic and acanthotic

Spinous layer: intracellular edema

Enlarged cells with lots of clear cytoplasm and small nucleus

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10
Q

Two important tests for white lesions

A
  1. Scrape it
  2. Stretch it
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11
Q

DD of leukoedema

A
  • White sponge nevus
  • HBID
  • Chronic cheek biting
  • Lichen planus
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12
Q

What is the etiology of lichen planus

A

Unknown etiology, but it is NOT autoimmune

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13
Q

T/F Leukoedema has a patch and is elevated

A

FALSE

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14
Q

White sponge nevus

A

Keratin 4 or 13 mutation

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15
Q

Features of white sponge nevus

A
  1. BILATERAL
  2. NOT on skin
    1. Occurs on GI, genital, and oral tract
  3. Younger patients
  4. No pain
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16
Q

Histopathology of WSN

A
  1. Thick epithelium
  2. Parakeratosis
  3. Acanthosis
  4. Perinuclear eosinophilic condensation of cytoplasm of prickle cells
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17
Q

HBID stands for:

A

Hereditary benign intraepithelial dyskeratisis

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18
Q

Who does HBID happen in

A

Triracial isolate: Caucasian, Native American, and AA in North Carolina

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19
Q

Key clinical feature of HBID

A
  1. Bulbar conjunctivitis
  2. Conjuctival plaques
  3. Foamy gelatinous plaques in the eye and orally
  4. White oral lesions
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20
Q

What mucosa involved in HBID

A

ANY mucosa including BILATERAL

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21
Q

Histopath of HBID

A

Hyperplasia

Acanthosis

Intracellular edema of the epithelium

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22
Q

Etiology of frictional keratosis

A

Chronic rubbing or friction

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23
Q

Clinical presentation of frictional keratosis

A
  • Gray or gray/white
  • Ill-defined margin
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24
Q

Common locations of frictional keratosis

A

Lip

Buccal mucosa

Tongue

Alveolar ridge

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25
Q

Histopath of frictional keratosis

A

Hyperkeratosis

Scattered inflammaroty cells in CT

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26
Q

Tobacco Pouch Keratosis etiology

A
  • Chronic smokeless tobacco use
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27
Q

Population high in tobacco pouch keratosis

A

White males

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28
Q

Clinical features of TPK

A
  • Color: grey-white
  • Appearance: leathery with fissured surface
  • Location: mandibular buccal fold
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29
Q

Histopath of TPK

A
  • Hyperkeratosos
  • Acanthosis
  • Parakeratin chevrons
  • Basophilic stromal alteration next to salivary glands
  • Occasional dysplasia
    • SCC possible
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30
Q

Nicotine stomatitis etiology

A
  • Pipe/cigar smokin’
  • Drinking hot coffee/tea
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31
Q

Nicotine stomatitis clinical features

A
  • Men > 45 years
  • Gray or white palatal mucosa
  • Papules with punctate red centers
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32
Q

Histopath of nicotine stomatitis

A
  • Hyperkeratosis
  • Acanthosis
  • Salivary glands with hella inflame
  • Excretory ducts squamous metaplasia
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33
Q

Hairy leukoplakia etiology

A
  • EBV VIRUS
  • Homosexual men with HIV/AIDS
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34
Q

Hairy leukoplakia clinical features

A
  1. Flat white plaques
  2. Vertical white corrugated lines on side of tongue
  3. Unilateral or bilateral
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35
Q

Hairy leukoplakia histopath

A
  • Hyperkeratosis
  • Beading of the nuclei in upper keratinocytes
  • Paucity of inflame cells
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36
Q

DD of hairy leukoplakia

A
  1. Idiopathic leukoplakia
  2. Frictional keratosis
  3. Lichen planus
  4. Hyperplastic candidiasis
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37
Q

Hairy tongue clinical appearance and features

A
  • Asymptomatic hyperplasia of filiform papillae
  • Thick, matted surface
  • Gagging or tickling
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38
Q

Etiology of dentrifrice-associated sloughing

A
  • Superficial chemical burn
  • Reaction to SLS in tooth paste
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39
Q

What is the tissue like underneath dentifrice associated slough?

A

Normal under the tissue

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40
Q

Clinical features of dentrifrice-associated sloughing

A
  • Superficial, white sloughing
  • Painless
  • Responds after switch toothpaste
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41
Q

Actinic cheilitis etiology

A

Chronic exposure to UV light

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42
Q

Actinic cheilitis clinical features

A

Color: pale to silver/grey

Appearance:

  • Fissured or glossy
  • Irregular with white diffuse thickening
  • Superical scaling, cracking, crusting

Painless and chronic

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43
Q

Treatment actinic cheilitis

A

Lip protection

Biopsy if persistent

  • 10% of cases = malignant SCC
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44
Q

Location of actinic cheilitis

A

Lower lip

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45
Q

Histopath of actinic cheilitis

A
  1. Epidermis: atrophic and hyperkeratotic
  2. Frequent dysplasia
  3. Solar elastosis in the submucosa
46
Q

Definition of leukoplakia

A

A white patch which cannot be wiped off or characterized as any other disease

47
Q

T/F Leukoplakia is always a clinical diagnosis

A

True. Histo diagnosis will never be leukoplakia

48
Q

Percentage of malignant transformation and hyperkeratosis to dysplasia in leukoplakia

A

malignant transformation: 10-15%

hyperkeratosis to dysplasia: 5-25%

49
Q

Etiology of leukoplakia

A
  • Tobacco and alcohol abuse
  • C. albicans
  • Nutrition deficiency
50
Q

Average age of leukoplakia

A

40 years old

51
Q

Common locations of leukoplakia

A
  1. Tongue
  2. Mandibular mucosa
  3. Buccal mucosa
  4. Floor of mouth
52
Q

Clinical features of leukoplakia

A

Appearance

  • Well defined borders
  • Flat slightly raised
  • Verrucous or wartlike
  • Granular or speckled with red spots
  • Can be rough or soft and smooth
53
Q

What is proliferative verrucous leukoplakia?

A

Multiple irregular white plaques

It is persistent, multifocal and aggressive with malignant transformation of 80-100%.

54
Q

DD of leukoplakia

A
  1. Candidiasis
  2. Frictional keratosis
  3. Lichen planus
  4. Lupus erythematosus
  5. Hairy leukoplakia
55
Q

Histopath of leukoplakia

A
  • Hyperkeratosis
  • Acanthosis
  • Dysplasia
    1. Teardrop rete ridges
    2. Basilar hyperplasia
    3. Maturational disturbances
    4. Dskeratotoci cells
  • Cellular Changes
    1. Enlarged cells/nuclei
    2. Hyperchromatism and pleomorphisms
56
Q

Degrees of Dysplasia in Leukoplakia

A
  1. Mild
    • Basailar 1/3
  2. Moderate
    • Basialr 1/2
  3. Severe
    • Cell alterations basilar 2/3 of epithemlium
  4. Carcinoma in situ
    • Full thinkness change. No invasion.
57
Q

Etiology of hairy tongue

A
  • Antibiotics
  • Oxygenating mouth washes
  • Intense smoking
58
Q

Onset of HBID

A
  • Early onset
  • Usually in the first year
59
Q

Microscopic appearance percentages of leukoplakia

A
  • 80% – hyperkeratosis and acanthosis
  • 12% – dysplasia
  • 3% – carcinoma in situ
  • 5% – squamous cell carcinoma
60
Q

Treatment for Leukoplakia

A
  1. STOP smoking or alcohol use
  2. Biopsy/excision/laser removal
  3. COX2 inhibitors
61
Q

How long does transformation to malignancy of leukoplakia take?

A

2-4 years with granular/veruciform being the greatest risk

62
Q

T/F after excision leukopakia is regularly followed up

A

True

63
Q

Cause of geographic tongue

A

Unknown

64
Q

Geographic tongue is associated with:

A
  • Psoriasis
  • Reiter’s syndrome
  • Seborrheic dermatitis
65
Q

Another name for geogrpahic tongue

A

Erythema migrans

66
Q

Clinical appearance of Geo tongue

A
  • Artophic patches surrounded by elevated keratotic margins (WHITE MARGINS)
  • Areas move around and change appearance
  • CAN be associated with fissured tongue
67
Q

Symptoms and location of geo tongue

A
  • USUALLY asymptomatic
  • Occasional complain of burning or tenderness
  • Floor of mouth, buccal mucosa, palate
68
Q

A biopsy is need for geo tongue

A

False

69
Q

Histopath of geo tongue

A

White margins: hyperkeratosis + acanthosis

Center red area: loss of keratin, intraepitheliala neutrophils

70
Q

Treatment of geo tongue

A
  1. MAGIC mouthwash
  2. Can use topical steroids
71
Q

Cause of lichen planus

A

Unknown cause.

Immunologically mediated

Increase in cytokines in the basement membrane

72
Q

Clinical features of lichen planus

A
  • Middle aged men and women
  • Skin and oral lesions
  • Keratinocytes killed by CD4/8 T cells
73
Q

What are the P’s of lichen planus

A
  1. Puritic
  2. Papular
  3. Purple
  4. Plaques
74
Q

What are the forms of lichen planus

A
  1. Reticular form
  2. Plaque
  3. Erythematous
  4. Erosive
75
Q

Describe the reticular and plaque forms of lichen planus

A
  • Reticular
    • White keratotic lines – WICKHAM’S STRIAE
    • Lacy pattern
    • Seen bilaterally on the cheeks. Can be on tongue or gingiva
  • Plaque
    • Slightly elevated to smooth and flat plaques
    • Resembles leukoplakia
    • Multiple present
76
Q

Describe the steps in lichen planus disease mechanism

A
  1. Initiating event
  2. Focal release of cytokines
  3. Upregulation of vascular adhesion molecules
  4. Recruitment of T cells
  5. Cytotoxocity of basal keratinocytes mediated by T cells
77
Q

Important histopath of lichen planus (think of immunologic events)

A
  • Hyperkeratosis
  • Degenration of the basal cell layer
  • Saw tooth rete rides
  • Dense BAND-LIKE inflammatory infiltrate in subepithelial region
78
Q

Describe the DIF of lichen planus

A

Presence of FIBRINOGEN at the basement membrane zone

79
Q

Describe the erythematous and erosive LP forms

A
  • Erythematous
    • Red patches with white striae
    • Attached gingiva commonly involved
    • Can feelin burning, discomfort
  • Erosive
    • Central area is ulcerated
    • Keratotic straie adjacent to erosive site
80
Q

Name a variant of lichen planus

A
  • Bullous lichen planus
    • Short lived with painful ulcers developing
    • Usually on buccal mucosa
81
Q

LP treatment

A
  • No cure, just control of disease
  • Topical and systemic corticosteroids
  • Immunosuppressive medications
  • Topical tacrolimus
82
Q

Lichen planus is an acute disease

A

False

83
Q

Forms of lupus erythematosus (LE)

A
  1. Systemic or acute (SLE)
  2. Localized or discoid (DLE)
84
Q

Etiology of LE

A
  • Autoimmune disease involving both humoral and cell-mediated immunity
  • Antibodies to nuclear antigens (ANA) present in serum and tissue
  • Also see circulating AN-AB complexes
85
Q

Typical person with DLE

A

Middle aged women

86
Q

Clinical Features of DLE

A
  • Skin
    • _​_Erythematous (red) plaques with hyperpigmented margins
  • Oral
    • Buccal mucosa, gingiva, vermilion most commonly involved
    • Erythematous and ulcerative lesions with white straie
87
Q

Clinical Features of SLE

A
  • Other organ systems
    • Joints
    • Lungs, kidney, heart
  • Systemic symptoms
    • Fever, weight loss, feel like poop
  • Oral
    • Vermilion, buccal mucoasa, gingiva
    • Erythemayous or ulcerative lesions with white straie
88
Q

DD of SLE

A
  • Lichen planus
  • When lesions erythemayous
    • MMP
    • Erosive lichen planus
    • Erythematous candidiasis
    • Contact hypersensitivity
89
Q

Histopath of LE

A
  • Hyperkeratosis with epithelial atrophy
  • Basal cell destruction
  • DIF with linear depositis of IgG, IgM, IgA, C3, and fibrinogen along the basement membrane
90
Q

Treatment of LE

A
  • Topical corticosteroids
  • Systemic steroids
  • Immunosupresives
  • Antimalrials
91
Q

Three non-epithelial white lesions studied

A
  1. Candidiasis
  2. Submucous fibrosis
  3. Mucosal burns
92
Q

Candidiasis is an oppurtunistic infection

A

True

93
Q

Define the acute and chronic types of candidiasis

A
  • Acute
    • Pseudomemranous
    • Atrophhic
    • Erythematous
  • Chronic
    • Hyperplastic
    • Atrophic
    • Angular cheilitis
94
Q

Predisposing factors of candidiasis

A
  • Dentures
  • Dry mouth
  • Diabetes
  • Antibiotic or steroid use
  • Immunopsuppresion – HIV, chemo, organ transplant
95
Q

Most common type of candidiasis

A

Pseudomembranous or thrush

96
Q

Describe pseudomembranous candidiasis

A
  • Young and elderly affected
  • White plaque that wipes off and leaves a red base underneath
97
Q

Appearance of erythemayous candidiasis

A

Bright red with a velvet or pebble surface

98
Q

DD of candiiasis

A
  • Red
    • Trauma
    • Drug reaction
    • Erosive lichen planus
    • LE
  • White
    • Chemical or trauma burn
    • Mucous patch of syphilous
    • White keratotoic plaques
99
Q

Treatment of candidiasis

A
  • Find the cause of it
  • Antifungal agents
    • Nystatin
    • Clotrimazole
100
Q

Etiology of oral submucous fibrosis (think if India)

A
  • Chewing betel quid
    • Causes impaired degeneration of normal collagen
101
Q

Clinical features of OSF

A
  • White/yellow change that has a chronic insidious route
  • Oral cavity loses its resilience and shows decreased vascularity and elastisity
  • Mucosal rigidity, pain, trismus
102
Q

Histopath of OSF

A
  • Hyperkeratosis
  • Atrophy of epithelia
  • Dense collagen deposits
  • Chronic inflammation
  • Dysplasia
  • SCC (6%)
103
Q

Treatment of OSF

A
  • Steroids
  • Eliminate the causitive agent
  • Surgical excision of bands
  • Close follow up
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Oral Pathology (5 decks)

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