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Dr. Bushra Nasir
In order to discuss pathologic lesions that are white, the first order is to eliminate the normal or variants of normal that appear white.
Leukoedema: Clinical Features
Occurs in 50%+ Whites and over 90% of African-Americans; uniform opacification of buccal mucosa bilaterally.
The cause of leukoedema is unknown.
Need to recognize; remains indefinitely; no ill effects.
One way white lesions can be classified is to separate them into two categories based upon whether the lesion can (pseudomembranesous or necrotic) or cannot (keratotic) be removed easily by rubbing or scraping them: 1. Pseudomembraneous or necrotic white lesions. 2. Keratotic white lesions.
Keratotic White Lesions
Leukoplakia (leuko-white; plakia-patch)
Oral leukoplakia is defined by the WHO as “a white patch or plaque that cannot be characterized clinically or pathologically as any other disease”. Thus a diagnosis by exclusion. The term is strictly a CLINICAL one and does not imply a specific histopathologic tissue alteration. Leukoplakia is the most common oral precancer.
The 15 Most Common Oral Pathoses
(Based on examination of 23,616 U.S. adults; excludes caries & periodontitis)
Number of Lesions per 1,000 Adults Diagnosis
Irritation fibroma Fordyce granules Torus mandibularis Leaf-shaped fibroma (under denture) Hemangioma Inflammatory ulcer Inflammatory erythema Papilloma Epulis fissuratum Lingual varicosities
3 4 5 6 7 8 9 10 11 12
13.0 17.7 9.6 0.4 8.4 5.4 4.5 5.3 3.4 3.5
11.4 5.2 7.9 12.9 4.1 5.1 4.8 4.2 4.4 3.4
11.9 9.7 8.5 6.7 5.6 5.2 4.7 4.6 4.0 3.5
Geographic tongue Papillary hyperplasia of palate
References: Bouquot JE. J Am Dent Assoc 1986; 112:50-57; www.oralpath.com
Leukoplakia: Why is it White?
The clinical color (white) results from a thickened surface keratin layer (which appears white when wet) and/or a thickened spinous layer, which masks the normal vascularity (redness) of the underlying connective tissue.
Leukoplakia: A Premalignant or Precancerous Lesion
Although leukoplakia is not associated with a specific histopathologic diagnosis, it is considered to be a premalignant lesion for the risk of malignant transformation is greater in a leukoplakic lesion than that associated with normal or unaltered mucosa.
Despite the fact that leukoplakia is a premalignant lesion it should be noted that not every lesion shows histopathologic evidence of epithelial dysplasia or frank malignancy (squamous cell carcinoma). In fact, dysplastic epithelium or invasive carcinoma is found in only 5 to 25 % of the biopsy samples of leukoplakia.
Leukoplakia: Malignant Transformation Potential
Overall, the malignant transformation potential of leukoplakia is 4 % (estimated lifetime risk). However, specific clinical subtypes are associated with much high potential malignant transformation rates (as high as 47 %).
Leukoplakia: How Common Is It?
Leukoplakia is by far the most common oral precancer, accounting for 85 % of such lesions. (Note: this statement is not saying that leukoplakia has the highest malignant transformation risk of the premalignant group of lesions for erythroplakia [erythroplasia] does). Leukoplakia is also a relatively common lesion for it is estimated that approximately 3 % of all white adults will be affected at some time. Additionally, Bouquot in his study of oral
Leukoplakia: Who Develops It?
There is a strong male predilection (70%), except in parts of the country where females use tobacco products more than males. Overall, there has been a slight decrease in the proportion of males affected over the past few decades. In general, leukoplakia is diagnosed more frequently now than in the past, probably because of enhance
The cause of leukoplakia remains unknown. Over the years the following have been considered: tobacco, alcohol, sanguinaria, ultraviolet radiation, microorganisms and trauma.
Etiology of Leukoplakia: The Role of Tobacco
The habit of tobacco smoking appears most closely associated with leukoplakia development. 80 % of patients with leukoplakia are smokers. Smokers are much more likely to have leukoplakia than non-smokers. Heavier smokers have greater numbers of and larger lesions than light smokers. A large proportion of leukoplakias in persons who stop smoking either disappear or
Etiology of Leukoplakia: The Role of Alcohol and Sanguinaria
Alcohol, which seems to have a strong synergistic effect with tobacco in oral cancer development, has not been associated with leukoplakia. Sanguinaria (blood root) is a herbal extract that has been used in toothpaste and mouthwash. Over 80 % of the patients with vestibular/maxillary alveolar leukoplakias have a history of using a sanguinaria containing product as compared to 3 % of the “normal” population; some lesions have
Etiology of Leukoplakia: The Role of Ultraviolet Radiation
Ultraviolet radiation has been associated with leukoplakia of the vermilion of the lower lip. This leukoplakia is usually associated with actinic cheilosis.
Etiology of Leukoplakia: The Role of Microorganisms
Treponema pallidum has been
implicated in leukoplakia of the dorsal surface of the tongue in patients with syphilis. Candida albicans has been demonstrated histologically in the hyperplastic/dysplastic epithelium of lesions termed candidal leukoplakia and candidal hyperplasia.
Etiology of Leukoplakia: The Role of Microorganisms Continued
Human papillomavirus (HPV), particularly subtypes 16 and 18, have been identified in some oral leukoplakias. However, HPV has also been demonstrated in normal oral epithelial cells.
Etiology of Leukoplakia: The Role of Trauma
Several keratotic lesions, which until recently have been viewed as variants of leukoplakia, are now considered not to be premalignant. Included in this group are lesions termed nicotine stomatitis and frictional keratosis. These keratoses are readily reversible after the elimination of the trauma or
Leukoplakia: Clinical Features
Leukoplakia usually affects people over the age of 40 years (average age is 60 years). Prevalence increases rapidly with age particularly in males. Approximately 8 % of the males over the age of 70 years are reportedly affected.
Leukoplakia: Clinical Features Continued
Approximately 70 % of the oral leukoplakias are found on the lip vermilion, buccal mucosa and gingiva. Note: Lesions of the tongue, lip vermilion and floor of the mouth account for more than 90 % of those that show dysplasia or carcinoma upon histologic examination.
Leukoplakia: Clinical Features Continued
Individual lesions vary in clinical appearance and tend to change over time. Early/mild lesions usually appear as slightly elevated gray or gray-white plaques, which may appear translucent, fissured or wrinkled and are typically soft and flat. Early/mild lesions are usually well demarcated but may blend into the
Leukoplakia: Clinical Features Continued
Early/mild thin leukoplakia, which seldom shows dysplasia on biopsy, may disappear or continue unchanged. If the cause (s) of the lesion are not removed, many lesions will gradually become thicker and larger. The clinical appearance (s) of leukoplakia and the anticipated underlying histopathologic changes are presented in the following diagram.
Proliferative Verrucous Leukoplakia (PVL)
PVL is a special high risk form of leukoplakia. It is characterized by multiple keratotic plaques with rough surface projections although initially beginning as a simple flat hyperkeratosis. PVL plaques tend to spread slowly, yet progressively. PVL usually transforms into a squamous cell carcinoma within about 8 years. PVL has a strong female predilection (1:4
Leukoplakia: Histopathologic Features
Leukoplakia is characterized by a thickened keratin layer (hyperkeratosis) with or without a thickened spinous layer (acanthosis). Some leukoplakias show surface hyperkeratosis but with atrophy or thinning of the underlying epithelium. Variable numbers of chronic inflammatory cells are typically noted within the underlying connective tissue.
Leukoplakia: Histopathologic Features Continued
While most leukoplakias show no dysplasia on biopsy, some 5 to 25 % of the cases do show evidence of epithelial dysplasia (or squamous cell carcinoma). The histopathologic alterations of dysplastic epithelial cells are outlined in the next slide.
Histopathologic Alterations of Dysplastic Epithelial Cells
Enlarged nuclei and cells. Large and prominent nucleoli. Increased nuclear-cytoplasmic ratio. Hyperchromatic (dark-staining) nuclei. Pleomorphic (abnormally shaped) nuclei and cells. Dyskeratosis (premature keratinization) Increased mitotic activity and abnormal mitotic figures
Histopathologic Alterations of Dysplastic Epithelium Continued
Bulbous or teardrop-shaped rete ridges. Loss of polarity (lack of progressive maturation toward the surface). Keratin or epithelial pearls. Loss of typical epithelial cell cohesiveness.
Leukoplakia: Treatment and Prognosis
Leukoplakia represents a clinical diagnosis and therefore the first step in treatment is to arrive at a definitive diagnosis via biopsy and histologic examination of the tissue. Treatment depends upon the diagnosis and any leukoplakia exhibiting moderate epithelial dysplasia or worse warrants complete removal if possible. Treatment of lesions exhibiting less severe changes is guided by the size of the lesion and its response to more conservative measures such as eliminating tobacco use.
Leukoplakia: Treatment and Prognosis Continued
Leukoplakia not exhibiting dysplasia often is not excised but clinical evaluation every 6 months is recommended. Additional biopsies are recommended if smoking continues or if clinical changes increase in severity. The following diagram represents the various clinical appearance of oral leukoplakia and the anticipated underlying associated histopathologic changes.
Leukoplakia: Treatment and Prognosis Continued
Complete removal of oral leukoplakia can be accomplished with equal effectiveness by surgical excision, electrocautery, cryosurgery or laser ablation. Long-term follow-up after removal is mandatory because of recurrence potential and because new leukoplakias may occur. Malignant transformation potential is related to clinical appearance and the degree of dysplasia present.
Nicotine Stomatitis: Clinical Features
Asymptomatic generalized opacification of palate with red dots representing inflamed salivary gland orifices scattered throughout.
Nicotine Stomatitis: Cause
Heat and smoke associated with combustion of tobacco; typically seen in pipe smokers.
Nicotine Stomatitis: Treatment
Discontinue smoking; lesion typically regresses.
Nicotine Stomatitis: Significance
Rarely develops into palatal cancer; malignant transformation risk no greater than for “normal” palatal mucosa.
Smokeless Tobacco Users Lesion
Snuff Dipper’s Lesion Tobacco Chewer’s Lesion
White Lesions Associated with Smokeless Tobacco:Clinical Features
Asymptomatic white folds surrounding area where tobacco is held; usually found in labial and buccal vestibules; a common oral lesion.
White Lesions Associated with Smokeless Tobacco: Cause
Chronic irritation from snuff or chewing tobacco.
White Lesions Associated with Smokeless Tobacco: Treatment
Discontinue habit; biopsy suspicious areas
White Lesions Associated with Smokeless Tobacco: Significance
Increased risk for development of verrucous and squamous cell carcinoma after many years.
Lichen planus is a relatively common, chronic dermatologic disease, often affecting the oral mucosa. Current evidence indicates it is an immunologically mediated disorder. Its relationship to stress is controversial. A variety of drugs are known to induce similar appearing lesions for which the term lichenoid mucositis is used.
Lichen Planus: Clinical Features
From 1 to 2 % of the population has cutaneous lichen planus. The majority of patients are middle-aged or older and there is a female gender predilection (3:2). Skin lesions appear as pruritic, purple, polygonal papules with a fine, lace-like network of white lines known as Wickham striae Oral and other mucous membranes may be
While many forms are recognized by some authors, there are essentially two forms of oral lesions: 1. Reticular lichen planus 2. Erosive lichen planus The white, keratotic lesion of the reticular form is what we are discussing today.
Reticular Lichen Planus
This is the more common form of the disorder. Usually it is asymptomatic and occurs most frequently on the buccal mucosae bilaterally. It may also affect the tongue, gingiva and palate as well as other areas. Reticular lichen planus was so named because of the interlacing white lines. However, the lesion may have a plaque like appearance.
Erosive Lichen Planus
This form is usually symptomatic due to ulceration. The lesions appear atrophic, erythematous with central areas of ulceration. Usually the fine, white, radiating striae can be seen at the edge of the lesion. With gingival involvement, this form is part of a group of specific disease entities, which produce a reaction
Lichenoid Drug Reaction Lichenoid Reaction
Lichen Planus: Histologic Features
The histologic features are characteristic but not pathognomonic because lichenoid mucositis and other lesions can appear similar. Orthokeratosis or parakeratosis is seen with the reticular form. The spinous layer may be atrophic or hyperplastic with “saw-toothed” rete ridges. The basal layer may show hydropic
Lichen Planus: Histologic Features Continued
A band-like infiltrate of predominantly Tlymphocytes adjacent to the epithelium is usually present. Degenerating keratinocytes (colloid, cytoid, hyaline or Civatte bodies) may be seen at the interface of the epithelium and connective tissue. Immunopathologic features are non-specific. Most lesions show a band of fibrinogen at the basement membrane zone.
Lichen Planus: Diagnosis
The diagnosis of the reticular form can often be made on clinical findings alone. Biopsy is often necessary to rule out other vesiculoerosive disease in cases of the erosive type.
Lichen Planus: Treatment and Prognosis
The reticular form typically produces no symptoms and requires no treatment. The erosive form is usually treated by topical (or systemic if necessary) corticosteroids. With steroid treatment, the patient should be monitored for candidal infection. Potential malignant transformation,
White Hairy Tongue
Hairy Tongue: Clinical Features
Elongation of filiform papillae; asymptomatic.
Hairy Tongue: Cause
Unknown; may follow antibiotic or corticosteroid use
Hairy Tongue: Treatment
Improve oral hygiene and identify contributing factors
Benign process; may be cosmetically objectionable.
(Squamous, Squamous Cell) Papilloma
Squamous Papilloma: Clinical Features
Painless, exophytic, granular to cauliflowerlike lesion; predilection for tongue, floor of mouth, palate, uvula, lips, faucial pillars; generally solitary; soft in texture; color is white or same as surrounding tissue; young adults and adults; is a common oral lesion. The squamous papilloma occurs in 1 in every 250 adults and makes up about 3% of the lesions sent for biopsy. We did about a 5 yr. study at MCV and had 464 lesions in our sample.
Squamous Papilloma: Cause
Most due to HPV; viral subtypes 6 and 11 have been detected in up to 50% of the oral papillomas.
Squamous Papilloma: Treatment
Squamous Papilloma: Significance
Lesion has no known malignant potential; recurrences are rare if properly excised.
(Oral) Verruca Vulgaris: Clinical Features
Painless, papillary, exophytic lesion usually with a white surface because of keratin production; may be regarded as a type of papilloma (Regezi, Sciubba and Jordan); children and young adults most effected; common on skin while uncommon intraorally.
Verruca Vulgaris: Cause
HPV with common subtypes being 2,4,6, and 40.
Verruca Vulgaris: Treatment
Oral lesions are treated by excision or obliterated with laser, cryotherapy, etc. Without treatment about 2/3 of the cases spontaneously regress with a couple of years.
Verruca Vulgaris: Significance
Of little significance; may be multiple and a cosmetic problem.
Verrucous Carcinoma: Clinical Features
Broad-based, exophytic, indurated lesion; usually found on buccal mucosa or in vestibule; adult males are most frequently affected
Verrucous Carcinoma: Cause
May be associated with use of tobacco, especially smokeless tobacco; HPV present in some lesions.
Verrucous Carcinoma: Treatment
Excision is treatment of choice; radiation may have a role in therapy today.
Verrucous Carcinoma: Significance
Slow-growing malignancy; welldifferentiated with better prognosis than usual squamous cell carcinoma; growth pattern is more expansile than invasive; metastases are uncommon.
White Sponge Nevus
Cannon’s Disease Familial White Folded Dysplasia
White Sponge Nevus: Clinical Features
Asymptomatic, bilateral, dense, shaggy, white or gray, generalized opacification; primarily buccal mucosa affected, but other membranes may be involved; rare entity.
White Sponge Nevus: Cause
Hereditary entity; autosomal dominant with high degree of penetrance and variable expressivity; keratin 4 and/or 13 affected (genes are mutated).
White Sponge Nevus: Treatment
White Sponge Nevus: Significance
Remains indefinitely; no ill effects.
Hairy Leukoplakia: Clinical Features
Filiform to flat patch on lateral tongue; often bilateral; occasionally on buccal mucosa; typically asymptomatic.
Hairy Leukoplakia: Cause
Opportunistic Epstein-Barr virus (EBV) infection.
Hairy Leukoplakia: Treatment
No specific treatment; patient should be evaluated for AIDS; may improve with AIDS therapy.
Hairy Leukoplakia: Significance
Seen in 20% of HIV-infected patients; marked increase in AIDS; may occur in non-AIDS-affected immunosuppressed patients and rarely in immunocompetent patients.
HEREDITARY BENIGN INTRAEPITHELIAL DYSKERATOSIS (HBID)
Synonym: Witkop-Von Sallmann Syndrome HBID is rare genodermatosis seen primarily in triracial isolate (African-American, White and Native American) originally discovered in NC. Autosomal dominant trait.
HBID: Clinical Features
Clinical Features: Usually appears during childhood. Oral and conjunctival lesions; oral lesions similar to white sponge nevus in appearance and location; milder cases resemble leukoedema. Ocular lesions appear as thick, opaque, gelatinous plaques affecting conjunctiva and sometimes cornea.
HBID: Clinical Features Continued
Eyes may tear, itch and patient may have photophobia. Plaques (eye) most prominent in spring and tend to regress in the fall. Blindness may occur from vascularity of cornea secondary to shedding of the plaque.
HBID: Histologic Features
Histologic Features: Hyperparakeratosis with acanthosis; upper spinous layers show a dyskeratotic process with epithelial cells appearing to be surrounded or engulfed by adjacent cells resulting in “cell-within-a-cell” phenomenon.
HBID: Treatment and Prognosis
No treatment is usually necessary for oral lesions. Patients with ocular lesions should see the ophthalmologist; plaques obscuring vision require surgery but they ultimately recur.
Synonyms: Keratosis Follicularis; Dyskeratosis Follicularis, Darier-White Disease. Uncommon autosomal dominant trait with high penetrance and variable expressivity. A lack of cohesion among surface epithelial cells characterizes the disease. A mutant gene that encodes an intracellular calcium pump has been identified as the cause for the abnormal desmosomal organization.
DARIER’S DISEASE: Clinical Features
Numerous erythematous, pruritic papules on trunk and scalp develop during second decade; lesions are rough and degradation of the accumulated keratin gives a foul odor. Palms and soles may exhibit pits and keratosis. The nails may show lines, ridges or painful splits.
DARIER’S DISEASE: Clinical Features Continued
Between 15% and 50% of patients have oral lesions, which are often multiple, normalcolored to white, flat- topped papules. ● If clustered together, the papules present a cobblestone appearance. ● The hard palate and alveolar mucosa are most commonly involved. ● Parotid swelling occurs in some patients.
DARIER’S DISEASE: Histologic Features
● ● ●
This is a dyskeratotic process characterized by a central keratin plug which overlies epithelium exhibiting a suprabasilar cleft The intraepithelial clefting is known as acantholysis and is not unique to Darier’s disease. The rete pegs are long, narrow and “test-tube shaped”. Dyskeratotic cells (corps ronds or grains) are observed.
DARIER’S DISEASE: Treatment and Prognosis
Photosensitive patients should avoid heat and sun exposure and use sunscreens. Systemic retinoids may be beneficial in severe cases. The condition is not premalignant.
A slowly developing, premalignant lesion of the lower lip that results from chronic or excessive UV light exposure. Much more common in light-complexioned persons who sunburn easily, this lesion is associated with those who have an outdoor occupation or hobby (therefore farmer’s/sailor’s lip). It has a similar pathophysiological and biological behavior as actinic keratosis. Patients are typically over the age of 40 and there is a strong male gender predilection. The earliest clinical changes include atrophy at the vermilion border characterized by a smooth surface
As the lesion progresses it becomes rough, scaly, thickened and may appear leukoplakic. Patient may indicate he can peel off the scale only to have it reform. With further progression, ulcers may develop and last several months. Many such changes may be irreversible but patient should be instructed to use lip balms with sunscreens to prevent further damage. Areas of thickening, ulceration, induration and leukoplakia should be biopsies. Vermilionectomy (lip shave) is the most popular method of treatment in those severe cases not showing malignant change. Since from 5-10 % of the cases undergo malignant change over time, long-term follow-up is necessary.
Sloughing, Pseudomembranous, Necrotic White Lesions
Acute Necrotizing Ulcerative Gingivostomatitis (ANUG)
Painful, elevated plaques (fungus) can be wiped off leaving an eroded, bleeding surface; associated with poor oral hygiene, systemic antibiotic therapy, systemic diseases, debilitation, reduced immune response; chronic infections may result in erythematous mucosa without obvious white colonies; common disease entity.
Pseudomembranous Candidiasis: Cause
Opportunistic fungus-Candida albicans; rarely caused by other Candida species.
Pseudomembranous Candidiasis: Treatment
Clotrimazole troches or nystatin suspension and treatment of the underlying cause.
Pseudomembranous Candidiasis: Significance
Usually disappears in 1 to 2 weeks after treatment; some chronic cases require long-term therapy.
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