Oral Pathology > White Lesions > Flashcards

White Lesions Flashcards

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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
Histopath of frictional keratosis
Hyperkeratosis Scattered inflammaroty cells in CT
26
Tobacco Pouch Keratosis etiology
* Chronic smokeless tobacco use
27
Population high in tobacco pouch keratosis
White males
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Clinical features of TPK
* Color: grey-white * Appearance: leathery with fissured surface * Location: mandibular buccal fold
29
Histopath of TPK
* Hyperkeratosos * Acanthosis * Parakeratin **_chevrons_** * Basophilic stromal alteration next to salivary glands * Occasional dysplasia * SCC possible
30
Nicotine stomatitis etiology
* Pipe/cigar smokin' * Drinking hot coffee/tea
31
Nicotine stomatitis clinical features
* Men \> 45 years * Gray or white palatal mucosa * Papules with punctate red centers
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Histopath of nicotine stomatitis
* Hyperkeratosis * Acanthosis * Salivary glands with hella inflame * Excretory ducts squamous metaplasia
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Hairy leukoplakia etiology
* **_EBV VIRUS_** * Homosexual men with HIV/AIDS
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Hairy leukoplakia clinical features
1. Flat white plaques 2. Vertical white corrugated lines on side of tongue 3. Unilateral or bilateral
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Hairy leukoplakia histopath
* Hyperkeratosis * Beading of the nuclei in upper keratinocytes * Paucity of inflame cells
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DD of hairy leukoplakia
1. Idiopathic leukoplakia 2. Frictional keratosis 3. Lichen planus 4. Hyperplastic candidiasis
37
Hairy tongue clinical appearance and features
* Asymptomatic hyperplasia of filiform papillae * Thick, matted surface * Gagging or tickling
38
Etiology of dentrifrice-associated sloughing
* Superficial chemical burn * Reaction to SLS in tooth paste
39
What is the tissue like underneath dentifrice associated slough?
Normal under the tissue
40
Clinical features of dentrifrice-associated sloughing
* Superficial, white sloughing * Painless * Responds after switch toothpaste
41
Actinic cheilitis etiology
Chronic exposure to UV light
42
Actinic cheilitis clinical features
**Color**: pale to silver/grey **Appearance**: * Fissured or glossy * Irregular with white diffuse thickening * Superical scaling, cracking, crusting Painless and **chronic**
43
Treatment actinic cheilitis
Lip protection Biopsy if persistent * 10% of cases = malignant SCC
44
Location of actinic cheilitis
Lower lip
45
Histopath of actinic cheilitis
1. Epidermis: atrophic and hyperkeratotic 2. Frequent dysplasia 3. Solar elastosis in the submucosa
46
Definition of leukoplakia
A white patch which cannot be wiped off or characterized as any other disease
47
T/F Leukoplakia is always a clinical diagnosis
True. Histo diagnosis will never be leukoplakia
48
Percentage of malignant transformation and hyperkeratosis to dysplasia in **leukoplakia**
malignant transformation: 10-15% hyperkeratosis to dysplasia: 5-25%
49
Etiology of leukoplakia
* _Tobacco_ and _alcohol_ abuse * C. albicans * Nutrition deficiency
50
Average age of leukoplakia
40 years old
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Common locations of leukoplakia
1. Tongue 2. Mandibular mucosa 3. Buccal mucosa 4. Floor of mouth
52
Clinical features of leukoplakia
Appearance * **_Well defined borders_** * Flat slightly raised * Verrucous or wartlike * Granular or speckled with red spots * Can be rough or soft and smooth
53
What is proliferative verrucous leukoplakia?
Multiple irregular white plaques It is persistent, multifocal and aggressive with malignant transformation of 80-100%.
54
DD of leukoplakia
1. Candidiasis 2. Frictional keratosis 3. Lichen planus 4. Lupus erythematosus 5. Hairy leukoplakia
55
Histopath of leukoplakia
* 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
Degrees of Dysplasia in Leukoplakia
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
Etiology of hairy tongue
* Antibiotics * Oxygenating mouth washes * Intense smoking
58
Onset of HBID
* Early onset * Usually in the first year
59
Microscopic appearance percentages of leukoplakia
* 80% -- hyperkeratosis and acanthosis * 12% -- dysplasia * 3% -- carcinoma in situ * 5% -- squamous cell carcinoma
60
Treatment for Leukoplakia
1. STOP smoking or alcohol use 2. Biopsy/excision/laser removal 3. COX2 inhibitors
61
How long does transformation to malignancy of leukoplakia take?
2-4 years with granular/veruciform being the greatest risk
62
T/F after excision leukopakia is regularly followed up
True
63
Cause of geographic tongue
Unknown
64
Geographic tongue is associated with:
* Psoriasis * Reiter's syndrome * Seborrheic dermatitis
65
Another name for geogrpahic tongue
Erythema migrans
66
Clinical appearance of Geo tongue
* Artophic patches surrounded by elevated keratotic margins (WHITE MARGINS) * Areas move around and change appearance * CAN be associated with fissured tongue
67
Symptoms and location of geo tongue
* USUALLY asymptomatic * Occasional complain of burning or tenderness * Floor of mouth, buccal mucosa, palate
68
A biopsy is need for geo tongue
False
69
Histopath of geo tongue
White margins: hyperkeratosis + acanthosis Center red area: loss of keratin, intraepitheliala neutrophils
70
Treatment of geo tongue
1. MAGIC mouthwash 2. Can use topical steroids
71
Cause of lichen planus
Unknown cause. Immunologically mediated Increase in cytokines in the basement membrane
72
Clinical features of lichen planus
* Middle aged men and women * Skin and oral lesions * Keratinocytes killed by CD4/8 T cells
73
What are the P's of lichen planus
1. Puritic 2. Papular 3. Purple 4. Plaques
74
What are the forms of lichen planus
1. Reticular form 2. Plaque 3. Erythematous 4. Erosive
75
Describe the reticular and plaque forms of lichen planus
* 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
Describe the steps in lichen planus disease mechanism
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
Important histopath of lichen planus (think of immunologic events)
* Hyperkeratosis * Degenration of the **basal cell layer** * Saw tooth rete rides * Dense BAND-LIKE _inflammatory_ _infiltrate_ in **subepithelial** region
78
Describe the DIF of lichen planus
Presence of **FIBRINOGEN** at the basement membrane zone
79
Describe the erythematous and erosive LP forms
* 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
Name a variant of lichen planus
* Bullous lichen planus * Short lived with painful ulcers developing * Usually on buccal mucosa
81
LP treatment
* No cure, just control of disease * Topical and systemic corticosteroids * Immunosuppressive medications * Topical tacrolimus
82
Lichen planus is an acute disease
False
83
Forms of lupus erythematosus (LE)
1. Systemic or acute (SLE) 2. Localized or discoid (DLE)
84
Etiology of LE
* 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
Typical person with DLE
Middle aged women
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Clinical Features of DLE
* _Skin_ * _​_Erythematous (red) plaques with hyperpigmented margins * _Oral_ * Buccal mucosa, gingiva, vermilion most commonly involved * Erythematous and ulcerative lesions with white straie
87
Clinical Features of SLE
* _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
DD of SLE
* Lichen planus * When lesions erythemayous * MMP * Erosive lichen planus * Erythematous candidiasis * Contact hypersensitivity
89
Histopath of LE
* Hyperkeratosis with epithelial atrophy * Basal cell destruction * **DIF with linear depositis of IgG, IgM, IgA, C3, and fibrinogen along the basement membrane**
90
Treatment of LE
* Topical corticosteroids * Systemic steroids * Immunosupresives * Antimalrials
91
Three non-epithelial white lesions studied
1. Candidiasis 2. Submucous fibrosis 3. Mucosal burns
92
Candidiasis is an oppurtunistic infection
True
93
Define the acute and chronic types of candidiasis
* Acute * Pseudomemranous * Atrophhic * Erythematous * Chronic * Hyperplastic * Atrophic * Angular cheilitis
94
Predisposing factors of candidiasis
* Dentures * Dry mouth * Diabetes * Antibiotic or steroid use * Immunopsuppresion -- HIV, chemo, organ transplant
95
Most common type of candidiasis
Pseudomembranous or thrush
96
Describe pseudomembranous candidiasis
* Young and elderly affected * White plaque that wipes off and leaves a red base underneath
97
Appearance of erythemayous candidiasis
Bright red with a velvet or pebble surface
98
DD of candiiasis
* Red * Trauma * Drug reaction * Erosive lichen planus * LE * White * Chemical or trauma burn * Mucous patch of syphilous * White keratotoic plaques
99
Treatment of candidiasis
* Find the cause of it * Antifungal agents * Nystatin * Clotrimazole
100
Etiology of _oral submucous fibrosis_ (think if India)
* Chewing betel quid * Causes impaired degeneration of normal collagen
101
Clinical features of OSF
* 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
Histopath of OSF
* Hyperkeratosis * **Atrophy** of epithelia * **Dense collagen deposits** * Chronic inflammation * Dysplasia * SCC (6%)
103
Treatment of OSF
* Steroids * Eliminate the causitive agent * Surgical excision of bands * Close follow up
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Oral Pathology
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