II Other White Lesions in the Oral Cavity

8/13/2019 II Other White Lesions in the Oral Cavity

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OTHER WHITE LESIONS

in the ORAL CAVITYMa. Bemerly P. Jardiolin-Sira, MD, FPSP

Pathologist


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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


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LEUKOEDEMAGeneralized opacificationEtiology: ? No established

associationSmoking, alcohol, bacterial

infection, electrochemical interactions havebeen implicated

Features: asymptomatic, symmetricallydistributed in the buccal mucosa

Histology: parakeratosis and acanthosis ofthe epithelium, with marked edema of thespinous cell layer


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LEUKOEDEMAWith stretching of the buccal mucosa, the

opaque changes disappear

Treatment: NO TREATMENT is necessarybecause the changes are innocuous, andTHERE IS NO MALIGNANT POTENTIAL


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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


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

condensation of the keratin NO treatment is needed== asymptomatic and benign


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WSN WSN


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Perinuclear condensation of the keratin


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HEREDITARY BENIGN INTRAEPITHELIALDYSKERATOSIS tkops disease Transmitted as AUTOSOMAL DOMINANT == rare!

By molecular analysis: defect is in the telomericregion 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 plaquesof the mucosa


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Affects the buccal, labial mucosa and labialcommissures, also the lateral surfaces of thetongue, 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 insome, BLINDNESS may occur due cornealvascularization


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Enlarged hyaline keratinocytes are thedyskeratotic elements, present in thesuperficial half of the epithelium

The lower spinous and the basal layers havenormal cellular features

Minimal inflammatory cell infiltrates

The same oral and conjunctival lesions


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Management: NO TREATMENT is needed Self-limiting and benign

No risk of malignant transformation


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FOLLICULAR KERATOSISAKA DariersDisease; Darier-WhiteDisease

Autosomal dominant disorderOnset: between 6-20 y.o

Disease has a predilection for the

skin, but 13% have oral lesions


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Skin lesions: small, papular lesionssymmetrically distributed over the face, trunkand intertriginous areas = goosebumps orchicken skin appearance

Papules coalesce and feel greasy due toexcessive keratin production

The coalesced areas form patches ofvegetating to verrucous growths that have a

tendency to become infected and malodorousMay occur unilaterally or in a zosterform

pattern

With fingernail changes: fragile, splinter and

subungal keratosis


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Goosebumps look Papules


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Human skinChicken Skin withoutFeathers


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Classic nail changesDariersDisease, NailChange


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Oral Lesions: favored sites are the attachedgingiva and hard palate

Appearance: small, whitish lesions withoverall COBBLESTONE appearance

Extension of the oral lesions to theoropharynx and pharynx may occur, causingobstruction = respiratory compromise


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http://www.google.com.ph/imgres?q=follicular+keratosis+pictures&start=311&hl=en&sa=X&tbo=d&rlz=1T4ADFA_enPH408PH413&biw=1360&bih=534&tbm=isch&tbnid=mukw8g_zg44nZM:&imgrefurl=https://www.healthtap.com/topics/follicular-hyperkeratosis-pictures&docid=N31l74WCUPeG5M&imgurl=https://s3.amazonaws.com/healthtap-public/ht-staging/user_answer/avatars/431759/large/open-uri20121006-15708-1yam5ft.jpeg?1349526143&w=280&h=259&ei=kKK8UMnbI4O6iQfiiYCIBg&zoom=1&iact=hc&vpx=2&vpy=173&dur=1154&hovh=207&hovw=224&tx=119&ty=120&sig=115623116341977932394&page=17&tbnh=145&tbnw=154&ndsp=21&ved=1t:429,r:0,s:311,i:73


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Oral lesions are similar to skin lesions!!! Features:

1. suprabasal lacunae or clefts formationcontaining acantholytic epithelial cells

2. Basal layer proliferation immediately belowand adjacent to the clefts

3. Formation of vertical clefts that show alining of parakeratotic and dyskeratotic cells

4. Presence of specific benign dyskeratoticcells called corps ronds and grains


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


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Corps ronds Corps grains


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Treatment: Vitamin A analogs or the retinoidsbut not long term therapy

The keratosis treatment may consist ofmoisturizing or keratolytic treatments

including: urea, lactic acid, salicylic acid, ortopical retinoids(retin A)
http://en.wikipedia.org/wiki/Ureahttp://en.wikipedia.org/wiki/Lactic_acidhttp://en.wikipedia.org/wiki/Salicylic_acidhttp://en.wikipedia.org/wiki/Retinoidshttp://en.wikipedia.org/wiki/Retinoidshttp://en.wikipedia.org/wiki/Salicylic_acidhttp://en.wikipedia.org/wiki/Lactic_acidhttp://en.wikipedia.org/wiki/Urea


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Sunscreen, loose cool clothing, and avoidinghot environments and usually preventuncomfortable outbreaks. Moisturizingcreams that have urea or lactic acid can

reduce scaling and hyperkeratosis. Forinflammation, a topical mid-potency steroidcan help. There are also treatments such astopical creams, injections, and oral

medications that deal with uncomfortablesymptoms of follicular keratosis.
http://www.skintreatmentcream.com/follicular/http://www.skintreatmentcream.com/follicular/http://www.skintreatmentcream.com/follicular/


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For more serious cases, surgical options are alsooffered. Electrosurgeryis more commonly usedto treat localized keratosis follicularis. Newtreatment methods using carbon dioxide lasersalso help to reduce symptoms. A combination

treatment using carbon dioxide lasers, curettageand shavingcan lead to longer remissionperiods. Combination treatments can keep thesymptoms at bay for up to 2 years.

Photodynamic therapy is done with a type of acidthat has proven effective in about 68 percent ofpatients and can improve or clear lesions for upto 3 years.


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ORAL WHITE LESIONS


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RELATED TO CHRONIC RUBBING Friction against an oral mucosal surface

Presumably protective hyperkeratosis

Analogous to CALLUSof 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


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Primary microscopic change:HYPERKERATOSIS

Diagnosis and Management:Careful history taking and careful diagnosis

Traumatic cause: NO BIOPSY; discontinue thehabit; offending tooth or denture should besmoothed

If causative, the lesion should be resolved orat least reduced in intensity with time

NO MALIGNANT POTENTIAL!!!


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ALL forms of smokeless tobacco maypotentially cause alterations in theoral mucosa

But SNUFF (finely divided or shreddedtobacco) appears to be much moreclosely related to cause oral lesions

than CHEWING Tobacco


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Oral mucosa responds to the topicallyinduced effects of tobacco == inflammationand 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 ofthree (3) tins of tobacco/week or duration ofthe habit for more than 2years


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Develop in immediate areas where tobacco ishabitually placed: mucobuccal fold of themandible in either the incisor or the molarregions

Mucosa appears granular or wrinkled; heavyand folded character in advanced cases

Microscopic: parakeratosis; edema orvacoulation of the epithelium; inflammation;dysplasia


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Discontinuation of tobacco use - may causesome lesions to disappear in weeks ormonths

Biopsy is necessary for persistent lesions Long period of exposure to smokeless

tobacco increases the risk of transformationto verrucous or squamous cell carcinoma


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ASSOCIATED WITH pipe and cigar smoking Positive and direct correlation between

intensity of smoking, and severity ofcondition

Tobacco carcinogen and HEAT== synergisticeffect in causing the stomatitis

Reverse smoking?


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Initially: erythematous change followed bykeratinization

Red dots surrounded by white keratotic rings


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Epithelial hyperplasia and hyperkeratosis ofthe epithelium

The salivary glands around the area affectedshow inflammatory change, and the excretory

ducts show squamous metaplasia


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Nicotine stomatitis may indicate an increasedrisk of epithelial dysplasia and neoplasiaelsewhere in the oral cavity, oropharynx, andupper respiratory tract

A potential indicator of significant epithelialchange at sites other than the hard palate


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Hairy leukoplakia

II Other White Lesions in the Oral Cavity

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