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OTHER WHITE LESIONS in the ORAL CAVITY

Ma. Bemerly P. Jardiolin-Sira, MD, FPSP Pathologist

Thickened keratin layer Intracellular epithelial edema Reduced vascularity of subjacent connective tissue

YELLOW WHITE LESIONS

Fibrin exudate over an ulcer Submucosal deposits Surface debris Fungal colonies

LEUKOEDEMA Generalized opacification Etiology: ? No established associationSmoking, alcohol, bacterial infection, electrochemical interactions have been implicated Features: asymptomatic, symmetrically distributed in the buccal mucosa Histology: parakeratosis and acanthosis of the epithelium, with marked edema of the spinous cell layer

LEUKOEDEMA With stretching of the buccal mucosa, the opaque changes disappear Treatment: NO TREATMENT is necessary because the changes are innocuous, and THERE IS NO MALIGNANT POTENTIAL

WHITE SPONGE NEVUS (wsn) Autosomal Dominant Asymptomatic, folded, white lesions affecting several mucosal sites Thickened lesions with spongy consistency Bilateral and symmetrical Appears early in life, before puberty

WHITE SPONGE NEVUS


Greatly thickened epithelium, with marked spongiosis, acanthosis, and parakeratosis With also marked hydropic or clear cell change, from the parabasal region and extending very close to the surface Characteristic cytologic feature: perinuclear eosinophilic

condensation of the keratin

NO treatment is needed== asymptomatic and benign

WSN

WSN

Perinuclear condensation of the keratin

HEREDITARY BENIGN INTRAEPITHELIAL DYSKERATOSIS Witkops disease Transmitted as AUTOSOMAL DOMINANT == rare! By molecular analysis: defect is in the telomeric region of chromosome 4q35 Clinically, starts at early age of life early onset =first year of life Bulbar ocular lesions with oral white lesions Ocular = gelatinous plaques causing conjunctivitis Oral = soft, asymptomatic, white folds and plaques of the mucosa

Affects the buccal, labial mucosa and labial commissures, also the lateral surfaces of the tongue, gingiva and palate But the dorsum of the tongue is spared !!! Gradual increase in the intensity of the oral lesions until midadolscence Ocular lesions may undergo spontaneous shedding of the conjunctival plaques, BUT in some, BLINDNESS may occur due corneal vascularization

Enlarged hyaline keratinocytes are the dyskeratotic elements, present in the superficial half of the epithelium The lower spinous and the basal layers have normal cellular features Minimal inflammatory cell infiltrates The same oral and conjunctival lesions

Management: NO TREATMENT is needed Self-limiting and benign No risk of malignant transformation

FOLLICULAR KERATOSIS

AKA

Dariers Disease; Darier-White Disease Autosomal dominant disorder Onset: between 6-20 y.o Disease has a predilection for the skin, but 13% have oral lesions

Skin

lesions: small, papular lesions symmetrically distributed over the face, trunk and intertriginous areas = goosebumps or chicken skin appearance Papules coalesce and feel greasy due to excessive keratin production The coalesced areas form patches of vegetating to verrucous growths that have a tendency to become infected and malodorous May occur unilaterally or in a zosterform pattern With fingernail changes: fragile, splinter and subungal keratosis

Goosebumps look

Papules

Human skin

Chicken Skin without Feathers

Classic nail changes

Dariers Disease, Nail Change

Oral Lesions: favored sites are the attached gingiva and hard palate Appearance: small, whitish lesions with overall COBBLESTONE appearance Extension of the oral lesions to the oropharynx and pharynx may occur, causing obstruction = respiratory compromise

Oral lesions are similar to skin lesions!!! Features: 1. suprabasal lacunae or clefts formation containing acantholytic epithelial cells 2. Basal layer proliferation immediately below and adjacent to the clefts 3. Formation of vertical clefts that show a lining of parakeratotic and dyskeratotic cells 4. Presence of specific benign dyskeratotic cells called corps ronds and grains

Corps ronds large, keratinized squamous cells with round, eosinophilic cytoplasm Corps grains smaller parakeratotic cells with pyknotic and hyperkeratotic nuclei

Corps ronds

Corps grains

Treatment: Vitamin A analogs or the retinoids but not long term therapy The keratosis treatment may consist of moisturizing or keratolytic treatments including: urea, lactic acid, salicylic acid, or topical retinoids (retin A)

Sunscreen, loose cool clothing, and avoiding hot environments and usually prevent uncomfortable outbreaks. Moisturizing creams that have urea or lactic acid can reduce scaling and hyperkeratosis. For inflammation, a topical mid-potency steroid can help. There are also treatments such as topical creams, injections, and oral medications that deal with uncomfortable symptoms of follicular keratosis.

For more serious cases, surgical options are also offered. Electrosurgery is more commonly used to treat localized keratosis follicularis. New treatment methods using carbon dioxide lasers also help to reduce symptoms. A combination treatment using carbon dioxide lasers, curettage and shaving can lead to longer remission periods. Combination treatments can keep the symptoms at bay for up to 2 years. Photodynamic therapy is done with a type of acid that has proven effective in about 68 percent of patients and can improve or clear lesions for up to 3 years.

ORAL WHITE LESIONS

RELATED TO CHRONIC RUBBING Friction against an oral mucosal surface Presumably protective hyperkeratosis Analogous to CALLUS of the skin Occurs in areas in that frequently traumatized: lips; lateral lines of the tongue; buccal mucosa along the occlusal line; edentulous ridges Chronic chewing is also a reason

Diagnosis Careful

Primary microscopic change: HYPERKERATOSIS

and Management:

history taking and careful diagnosis Traumatic cause: NO BIOPSY; discontinue the habit; offending tooth or denture should be smoothed If causative, the lesion should be resolved or at least reduced in intensity with time NO MALIGNANT POTENTIAL!!!

ALL forms of smokeless tobacco may potentially cause alterations in the oral mucosa But SNUFF (finely divided or shredded tobacco) appears to be much more closely related to cause oral lesions than CHEWING Tobacco

Oral mucosa responds to the topically induced effects of tobacco == inflammation and keratosis Dysplastic changes follow == LPM Carcinogenic factors in the snuff: NITROSONORNICOTINE; pH between 8.2-9.3 Duration of exposure is also a factor: measured in terms of years Leukoplakia can be predicted with the use of three (3) tins of tobacco/week or duration of the habit for more than 2years

Develop in immediate areas where tobacco is habitually placed: mucobuccal fold of the mandible in either the incisor or the molar regions Mucosa appears granular or wrinkled; heavy and folded character in advanced cases Microscopic: parakeratosis; edema or vacoulation of the epithelium; inflammation; dysplasia

Discontinuation of tobacco use - may cause


some lesions to disappear in weeks or months

Biopsy is necessary for persistent lesions!!! Long period of exposure to smokeless tobacco increases the risk of transformation to verrucous or squamous cell carcinoma

ASSOCIATED WITH pipe and cigar smoking Positive and direct correlation between intensity of smoking, and severity of condition Tobacco carcinogen and HEAT== synergistic effect in causing the stomatitis Reverse smoking?

Initially: erythematous change followed by keratinization Red dots surrounded by white keratotic rings

Epithelial hyperplasia and hyperkeratosis of the epithelium The salivary glands around the area affected show inflammatory change, and the excretory ducts show squamous metaplasia

Nicotine stomatitis may indicate an increased risk of epithelial dysplasia and neoplasia elsewhere in the oral cavity, oropharynx, and upper respiratory tract A potential indicator of significant epithelial change at sites other than the hard palate

Hairy leukoplakia