White Lesions of the Oral Cavity

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These Question-and-Answer flashcards summarize definitions, clinical features, etiologies, and management pearls for hereditary, reactive, immunologic, infectious, systemic, premalignant, and neoplastic white lesions of the oral cavity covered in Dr. Otakhoigbogie’s lecture.

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47 Terms

1
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What are the four main histologic reasons an oral mucosal lesion appears white?

A thickened keratin layer, epithelial hyperplasia, intracellular epithelial edema, and/or reduced vascularity of the underlying connective tissue.

2
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Besides tissue alterations, what surface-related factors can make an oral lesion look white or yellow-white?

Fibrin exudate covering an ulcer, submucosal deposits, surface debris, or fungal colonies.

3
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Name the seven major classification groups of oral white lesions.

Hereditary/Developmental, Reactive, Immunologic, Infectious (Bacterial/Viral/Fungal), Systemic disease–related, Potentially malignant disorders, and Neoplastic.

4
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Which five conditions fall under the Hereditary/Developmental category of white lesions?

Leukoedema, White spongy nevus, Hereditary benign intraepithelial dyskeratosis (HBID), Pachyonychia congenita, and Dyskeratosis congenita.

5
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Give three common examples of Reactive white lesions.

Frictional keratosis, Morsicatio buccarum, and Nicotine stomatitis (also tobacco pouch keratosis and chemical burn).

6
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List two potentially malignant white disorders.

Leukoplakia and Actinic cheilitis.

7
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Which neoplastic white lesion is most clinically significant?

Oral squamous cell carcinoma (OSCC).

8
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How does leukoedema typically appear and respond to stretching?

As a diffuse grayish-white opalescent bilateral buccal mucosa change that fades or disappears when the mucosa is stretched.

9
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What treatment is required for leukoedema?

None; it is a benign anatomic variation.

10
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White spongy nevus inheritance pattern and typical onset?

Autosomal dominant; present at birth or in early childhood.

11
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Describe the oral presentation of white spongy nevus.

Asymptomatic, symmetrical, velvety or corrugated white plaques on bilateral buccal mucosa; may involve other mucosal sites.

12
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Does white spongy nevus need treatment?

No; it is benign.

13
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Hereditary benign intraepithelial dyskeratosis (HBID) affects which two sites?

Oral mucosa (corrugated white plaques) and bulbar conjunctiva (thick plaques).

14
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Who should manage the ocular component of HBID?

An ophthalmologist.

15
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What nail change is characteristic of pachyonychia congenita?

Tubular or thickened nails due to keratin accumulation in the nail beds.

16
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Which type of pachyonychia congenita shows oral lesions, and where do they occur?

Type I; thickened white plaques on the dorsum and lateral borders of the tongue.

17
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Dyskeratosis congenita is inherited in what pattern and shows what oral risk?

X-linked (male predilection); oral lesions may transform into squamous cell carcinoma.

18
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What triad is commonly associated with dyskeratosis congenita?

Oral bullae/erosions evolving to leukoplakia, dystrophic nails, and skin hyperpigmentation of face and neck.

19
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Define frictional keratosis and its expected course after irritant removal.

A rough white lesion caused by mechanical irritation; should resolve within two weeks once the irritant is eliminated.

20
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What management step is indicated if frictional keratosis persists beyond two weeks?

Biopsy to rule out epithelial dysplasia.

21
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Morsicatio buccarum is most often associated with what patient habit?

Chronic cheek biting, chewing, or sucking, frequently related to stress.

22
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Describe the typical appearance of morsicatio buccarum.

Bilateral shredded white patches on the anterior buccal mucosa along the occlusal line, sometimes with erythema or ulceration.

23
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What heat-related lesion develops on the palate of heavy smokers?

Nicotine stomatitis.

24
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What are the characteristic papules seen in nicotine stomatitis?

Elevated white papules with central red dots, representing inflamed salivary duct openings.

25
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How quickly does nicotine stomatitis reverse after smoking cessation?

Usually within two weeks.

26
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Where is tobacco pouch keratosis most commonly located?

Anterior mandibular vestibule and buccal sulcus at the site of tobacco placement.

27
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What feature gives tobacco pouch keratosis its name on stretching the mucosa?

A distinct 'pouch' caused by flaccid, chronically stretched tissue.

28
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What is the primary preventive measure for oral chemical burns during endodontic procedures?

Use of a rubber dam.

29
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Which immunologic disorder shows Wickham's striae?

Oral lichen planus (reticular form).

30
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Name two sites commonly affected by oral lichen planus besides buccal mucosa.

Tongue and gingiva (also palate).

31
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How does a lichenoid drug reaction differ clinically from classic lichen planus?

It mimics lichen planus but is linked to a drug or metal; lesions resolve after eliminating the offending agent.

32
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Describe the oral lesions of discoid lupus erythematosus (DLE).

Central erythematous zone surrounded by white radiating striae or hyperkeratotic plaques, usually asymmetric and accompanied by skin lesions.

33
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What oral pattern is typical of chronic graft-versus-host disease (GVHD)?

Fine reticular white striae similar to lichen planus or diffuse white papules involving cheeks, tongue, lips, and gingiva.

34
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Which two clinical types of candidiasis present as white lesions?

Pseudomembranous candidiasis and hyperplastic (candidal leukoplakia) candidiasis.

35
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How can pseudomembranous candidiasis be differentiated clinically from other white lesions?

Its white curd-like plaques can be readily scraped off, revealing erythematous mucosa.

36
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What laboratory finding confirms hyperplastic candidiasis?

Histologic presence of candidal hyphae in the epithelium.

37
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Describe the oral lesions of secondary syphilis.

Multiple painless grayish-white plaques (mucous patches) overlying ulcerated necrotic surfaces on tongue, gingiva, palate, or buccal mucosa.

38
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Oral hairy leukoplakia is caused by which virus and arises in what patient population?

Epstein-Barr virus (EBV) in severely immunodeficient patients (e.g., advanced HIV).

39
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Where is oral hairy leukoplakia classically located and what does it look like?

Lateral borders of the tongue; vertical white streaks or thick, furrowed white plaques.

40
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What breath odor may accompany uremic stomatitis and why?

Ammonia or urine-like odor due to elevated salivary urea broken down to ammonia.

41
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Provide the clinical definition of leukoplakia.

A white patch or plaque that cannot be characterized clinically or pathologically as any other disease.

42
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Differentiate homogeneous and non-homogeneous leukoplakia.

Homogeneous: uniform gray-white, slightly elevated, fissured plaques. Non-homogeneous: mixed color or textured variants such as speckled, nodular, verrucous, or proliferative verrucous leukoplakia.

43
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What is the approximate malignant transformation range reported for leukoplakia?

4% to 47%.

44
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Actinic cheilitis primarily affects which lip surface and is associated with what risk factor?

The vermilion border of the lower lip; chronic sun (UV) exposure.

45
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When a white patch clinically resembles leukoplakia, what procedure is mandatory to rule out invasive carcinoma?

Incisional or excisional biopsy.

46
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Why should patients with dyskeratosis congenita be placed on periodic recall?

To monitor for malignant transformation of oral lesions to squamous cell carcinoma.

47
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Which two topical agents are commonly used to manage oral lesions in GVHD and DLE?

Topical corticosteroids and (for GVHD) tacrolimus.