White Lesions

Question 1

Leukoedema

Answer 1

Hereditary Condition
mild opacification of the buccal mucosa of unknown etiology. The opaque changes dissipate when stretched. In rare cases textural changes can be seen
Epithelium is perakeratotic and acanthotic with intracellular edema of the spinous cells.
DD: white sponge nevus, hereditary benign intraepithelial dyskeratosis, cheek biting, lichen planus (differentiated microscopically)
No treatment but biopsy should be performed if diagnosis is in question

Question 2

White Sponge Nevus (Cannon’s Disease)

Answer 2

Asymptomatic, folded, white lesion in several mucosal sites. Lesions tend to be thickened and have a spongy consistency, typically bilateral and symmetric, and appears typically pre-puberty.
Microscopically the epithelium is thickened, with marked spongiosis, acanthosis, and parakeratosis. perinuclear eosinophilic condensation of cytoplasm is characteristic of prickle cells.
DD: hereditary benign epithelial dyskeratosis, lichen planus, lichenoid drug reaction, lupus erythematosus, cheek chewing, candidiasis.
No treatment necessary after biopsy

Question 3

Hereditary Benign Intraepithelial Dyskeratosis

Answer 3

rare hereditary condition. Early Onset, bulbar conjunctivitis, conjunctival plaques, and oral white lesions.
Oral lesions are soft, asymptomatic, white folds and plaques of spongy mucosa, usually in the buccal and labial mucosa and labial commisures, and floor of the mouth, and lateral surfaces of the tongue. Typically begin in the first year of life.
Histopathologically, epithelial hyperplasia and acanthosis with intracellular edema.
No treatmetn is necessary

Question 4

Hereditary, does not disappear when stretched, biopsy to confirm, may also involve conjunctiva

Answer 4

White sponge Nevus and hereditary benign intraepithelial dyskeratosis

Question 5

Look for bilateral white reticulations (striae), erosions, atrophy, and associated skin lesions, Biopsy

Answer 5

Lichen Planus

Question 6

Look for white lesions, asymmetrical, in contrast with new drug history

Answer 6

Lichenoid drug reaction

Question 7

White shaggy lesions along occlusal plane or trauma sites

Answer 7

Cheek Chewing

Question 8

Delicate radiating straie. usually unilateral Biopsy

Answer 8

Lupus Erythematosus

Question 9

Look for predisposing factors, can rub off, responds to antifungal therapy

Answer 9

Candidiasis

Question 10

Follicular Keratosis

Answer 10

autosomal dominant disorder occurring between age 6-20. most have skin lesions, the oral lesions are small, skin-colored papular lesions, symmetrically distributed over the skin that parallel the oral lesions. Typically small, whitish papules, producing a cobbelstone appearance.
Histopathology: suprabasal lacunae containing acanthotic epithelial cells, basal layer proliferation below the lacunae, formation of vertical clefts that show a lining of parakeratotic and dyskeratotic cells, and the presence of specific benign dyskeratotic cells.
Treatment: topical corticosteroids and vitamin A, but long term therapy is tolerated poorly.

Question 11

Focal (frictional) hyperkeratosis

Answer 11

a white lesions related to chronic fubbing or friction, causing a hyperkeratotic white lesion. commonly traumatized areas such as lips and lateral margin of the tongue, buccal mucosa, and edentulous alveolar ridges.
Histopathology: hyperkeratosis
Diagnosed by careful history, and removing the source should resolve the lesion or reduce in intensity over time. Biopsy if in doubt.
No treatment required, patient to control the habit.

Question 12

Determine cause (ill fitting dentures, trauma), biopsy

Answer 12

Frictional Keratosis

Question 13

White lesion of unknown origin. Assess risk factors and biopsy

Answer 13

Dysplasia, in situ carcinoma, SSC

Question 14

History of aspirin or other agent application to site of lesion, food injury

Answer 14

Burn (chemical or food)

Question 15

Lateral borders of tongue, irregular surface architecture, often bilateral, frequently with immunosuppression. Biopsy

Answer 15

Hairy Leukoplakia

Question 16

White lesions associated with smokeless tobacco

Answer 16

clinical results in development of white patches in the labial mucosa with a slight increase in malignant potential. acceleration of periodontal disease and dental abrasion are common.
Histopathology: slight to moderate perakeratosis. Superficial epithelium may demonstrate vacuolization or edema. occasional epithelial dysplasia.
Discontinuation of smokeless tobacco will frequently improve lesions. Persistent lesions should be biopsied.

Question 17

Nicotine Stomatitis

Answer 17

Palatal mucosa responds with an erythematous change followed by keratinization. Red dots surrounded by white keratotic rings appear, which is inflammation surrounding the minor salivary glands.
Histopathology characterized by epithelial hyperplasia and hyperkeratosis.
Denture can frequently block the formation. Low risk of dysplasia but an indicator for frequency of smoking

Question 18

Hairy Leukoplakia

Answer 18

an unusual lesion along the lateral margins of the tongue, related to an Epstein-Barr virus in immunosupressed individuals (HIV, organ transplant)
Well demarcated white lesion that varies in architecture from flat and plaque like to papillary/filiform, or a corrugated lesion. May be unilateral or bilateral.
Histopathology: Viral inclusions and/or peripheral displacement of chromatin with a smudgy nucleus is evident
DD: idiopathic leukoplakia, frictional hyperkeratosis, and leukoplakia associated with tobacco use
no treatment available, other than address immunosupression.

Question 19

Hairy Tongue

Answer 19

sometimes caused by broad-spectrum antibiotics and systemic corticosteriods, or peroxide mouth rinse in some cases.
Asymptomatic hyperplasia of the filiform papillae, resulting in a thick matted surface that traps bacteria, fungi, cellular debris, and foreign material.
Histopathology: elongated filiform papillae, with clusters of microorganisms and fungi.
identify abx of mouth rinse, brushing with baking soda or tongue scraper can reduce.

Question 20

Dentifrice-Associated Slough

Answer 20

Superficial white slough of the buccal mucosa, typically that easily wipes away. Associated with sanguinaria, resolves with discontinuation of the toothpaste/mouth rinse

Question 21

Actinic Cheilitis

Answer 21

Accelerated tissue degeneration of the vermilion of the lips. potentially pre-malignant condition.
the vermilion of ht elips takes on an atrophic, pale gray, glossy appearance. Slightly firm, bilatral swelling is common.
Histopathology: epitheium is typically atrophic and may show epithelial dysplasia. Basophilic changes in the submucosa
Treatment: Lip protection is indicated, with the use of lip balm containing a sunscreen agent indicated. Biopsy if ulceration persists (wedge excisional biopsy)

Question 22

Idiopathic Leukoplakia

Answer 22

A white patch or plaque that cannot be rubbed off and cannot be characterized clinically as any other disease (excludes lichen planus, candidiasis, leukoedema, WSN, and frictional keratosis). Biopsy is mandatory to establish definitive diagnosis.
Aproximately 5% are malignant at time of biopsy, and 5% of the remainder will become malignant.
THe floor of the mouth has few of these but a high percentage of dysplasia, carcinoma insitu, or invasive carcinoma.
Some have red zones (erythroleukoplakia) and are more frequently malignant.
DD: if lesion can be removed then it is a pseudomembrane, fungus colony, or debris. If bilateral then hereditary conditions, cheek chewing and lichen planus and lupus eruthematosis. Concomitant cutaneous lesions indicate the latter two. Frictional or tobacco associated should be considered. Hairly leukoplakia and geographic tongue.

Question 23

Geographic Tongue

Answer 23

seen in 2% of US population, young non-smokers. Atrophic patches surrounded by elevated keratotic margins. It is more common with a fissured tongue possibly due to secondary fungal infection.
Most are asympatomatic but some report irritation or tenderness to spicy foods or alcohol.
Histopathology: Filliform papillae are atrophic, with hyperkeratosis and acanthosis at the margins.
DD: generally clinical appearance is diagnostic, but biopsy may be required for an equivocal case, such as candidiasis, leukoplakia, lichen planus, and lupus erythematosus
No treatment required, but keeping the oral cavity clean with baking soda mouth rinse can help. Topical steroids with an antifungal can help

Question 24

Lichen Planus

Answer 24

Chronic mucocutaneous disease of unknown cause. 0.2-2% of population
Bilateral white lesions, occasionally with associated ulcers. Generally considered to be an immunologic process. Possibly preceded by dental materials, stress, drugs, infectious agents.
THe disease follows several steps: initiating factor/event, focal release of regulatory cytokines, upregulation of vascular adhesion molecules, recruitment of T cells, and cytotoxicity of basak keratninocytes mediated by T cells.
most common type is characterized by numerous interlacing white keratotic lines or striae that produce an annular or lacy pattern. The plaque form resembles leukoplakia clinically with a multifocal distribution, primarily on dorsum of tongue and buccal mucosa. Erythematous form has red patches with very fine white striae, where the central area of the lesion is ulcerated. A fibrinous plaque or pseudomembrane covers the ulcer.
Histopathology: hyperkratosis, basal layer vacuolization with apoptotic keratinocytes, and lymphophagocytic infiltrate at the epithelium-connective tissue interface. Sawtooth rete ridge pattern can be seen.
DD: lichenoid drug reaction, lupus erythematosus, white sponge nevus, hairy leukoplakia, cheek chewing, graft-versus-host disease, and candidiasis. Idiopathic leukoplakia or SSC could be considered. Erosive forms must be differentiated from cicatrical pemphigoid, pemphigus vulgaris, chronic LE, contact hypersensitivitym and chronic candidiasis.
Corticosteroids are the most useful treatment, topically appied, but do not cure.
There is a low risk of malignant transformation, usually with the erosive forms.

Question 25

Lupus Erythematosus

Answer 25

2 forms - Systemic Lupus Erythematosus (acute), and Discoid Lupus Erythematosus (Chronic)
DLE is characterized by cutaneous lesions (disc shaped cutaneous plaques) that expand and form a scar in the middle, and can result in alopecia. mucous membrane lesions occur in 3-25% of cases in the buccal mucosa, gingiva, and vermilion.
SLE is characterized by multiple organ involvement with limited skin and mucosal lesions. typically a butterfly rash over the nose is seen, although other areas may be involved. Oral lesions are similar to DLE and seen in 9-45% of cases. Ulceration, erythema and keratosis may be seen.
Histopathology: basal cell destruction, hyperkeratosis, epithelial atrophy, lymphocytic infiltration, and vascular dilation with edema of the submucosa are seen.
DD: erosive lichen planus, but less symmetrically distributed, and the striae are more delicate and subtle than lichen planus. It can be confused with mucous membrane pemphigoid, erythematous lichen planus, erythematous candidiasis, and contact hypersensitivity.
Treatment with topical corticosteroids

Question 26

Candidiasis

Answer 26

Can be related to immunosupression or short term use of systemic antibiotics.
Clinically it is an acute pseudomembranous form (thrush). Found in 5% of neonates, 5% of debilitated elderly, and 10% of institutionalized elderly, as well as radiation and chemotherapy.
Characteristic white, soft plaques that grow centrifugally and merge, and can be wiped away leaving a painful, erythematous, eroded or ulcerated surface. Eventually the pseudomembrane is lost, leading to a more generalized red lesion (acute erythematous candidiasis). Chronic candidal infections can produce a hyperplastic tissue response (candidial leukoplakia) which some believe is premalignant. hyperplastic candidiasis (median rhomboid glossitis) has an oval or rhomboid outline, smooth or nodular or fissured surface.
Histopathology: fungal hyphae seen penetrating the upper layers of epithelium at acute angles. Neutrophilic infiltration is often seen, alogn with epithelial hyperplasia
DD: chemical burns sough, traumatic ulcerations, mucocutaneous patches of syphilis, white keratotic lesions. Red lesions could be drug reactions, erosive lichen planus, and DLE
Treatment includes copical application of nystatin suspension, preferably in a cream or oimtment. IF there is hyperplastic lesions then systemic antifungans are indicated as well, or surgical management.

Question 27

Mucosal Burns

Answer 27

usually caused by topical application of chemicals, usually aspirin or alcohol mouth rinse.
localised mild erythema may occur, the longer the contact the more coagulative necrosis occurs, forming a white slough or membrane that will peel off. Temperature burns are more likely erythematous then white (chemical burns).
Histopatholgy: epithelial component shows coagulative necrosis through entire thickness with a fibrinous exudate.
local symptomatic therapy is aimed at keeping the area clean, bicarbonate mouthrinse can help.

Question 28

Submucous Fibrosis

Answer 28

usually nutritional deficiency or chronic exposure to dietary irritants (chili pepper/betel nut)
a whitish yellow change that has a chronic, insidious biological course. over time the affected mucosa (especially soft palate and buccal mucosa) loses resilience with limited vascularity and elasticity. This extends from the lamina propria to the musculature, causing trismus
Histopathology: principal feature is atrophy of the epithelium, and sub adjacent fibrosis. lamina propria is poorly vascularized with few fibroblasts.
Elimination of the causative agents is important. surgical interventions are only temporary. 1/3 will develop SSC

Question 29

Fordyce Granules

Answer 29

ectopic sebaceous glands. Lesions are asymptomatic and often discovered incidentally.
microscopically, lobules of sebaceous glands are aggregated around adjacent excretory ducts. Heterotropic glands are well formed and appear functional.
No treatment indicated

Question 30

Ectopic Lymphoid Tissue

Answer 30

most notably in the region surrounding the oropharynx (Waldeyer’s Ring)
Tissue appears yellow or yellow-white clinically, typically produces small dome-shaped elevations. Tissue is uninflamed the the patient is typically unaware of them.

Question 31

Gingival Cysts

Answer 31

neonatal gingival cysts arise from dental lamina remnants, that form cystification and keratin accumulation. in adults they are probably formed form remnants of the dental lamina within gingival submucosa. Cystic changes in these rests may occasionally result in a multilocular lesion.
Cysts appear off-shite colored nodules aprox 2mm in diameter, from one to many along the alveolar crests. midline palatally they can occur at the junction of the hard and soft palate. In adults they look similar to a periodontal cyst.
Histopathology: bland stratified squamous epithelium filled with keratinaceous debris.
No treatment required in infants. in adults surgical excision.

Question 32

Parulis

Answer 32

focus of puss in the gingiva, derived from an acute infection at the base of a periodontal pocket or the apex. Appears as a yellow/white gingival tumescence with associated erythema. symptoms are relieved when the pus escapes. Treatment of the underlying infection needed.