White lesions (2)

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WHITE LESIONS

Prepared by:Dr. Rea Corpuz

lesions of the oral mucosa, which are white results from a

thickened layer of keratin

epithelial hyperplasia

intracellular epithelial edema

reduced vascularity of subjacent connective tissue

White Lesions

white or yellow lesions may also be due to fibrous exudate covering an:

ulcer submucosal deposit surface debris fungal colonies

White Lesions

(1) Leukoedema

(2) Leukoplakia

(3) Lichen Planus

(4) Candidiasis

(5) White Sponge Nevus

(6) Nicotine Stomatitis

White Lesions

(7) Geographic Tongue

(8) Hairy Tongue

(9) Dental Lamina Cyst

(10) Fordyce’s Disease

(11) Perleche

White Lesions

generalized opacification of buccal mucosa that is regarded as a variation of normal

can be identified in majority of population

(1) Leukoedema

Etiology & Pathogenesis

to date, cause has not been established

smoking chewing tobacco none alcoholo ingestion are bacterial infection proven salivary condition cause electrochemical interactions have been implicated

(1) Leukoedema

Clinical Features

usual discovered as incidental finding

asymptomatic

symmetrically distributed in buccal mucosa

(1) Leukoedema

Clinical Features

appear as gray-white, diffuse, filmy or milky surface

more exaggerated cases, whitish cast with surface textural changes

• wrinkling• or corrugations

(1) Leukoedema

Clinical Features

with stretching of buccal mucosa, opaque changes dissipate

more apparent in non-whites, especially African-American

(1) Leukoedema

Treatment

NO treatment is necessary

since there is no malignant potential

if there is any doubt about diagnosis, a biopsy can be performed

(1) Leukoedema

also known as Leukokeratosis; Erythroplakia

Leuko= white

Plakia = patch

defined by World Health Organization (WHO) as a white patch or plaque that cannot be characterized clinically or pathologically as any other disease

(2) Leukoplakia

clinical term indicating a white patch or plaque of oral mucosa

cannot be rubbed off

cannot be characterized clinically as any other disease

biopsy is mandatory to establish a definitive diagnosis

Leukoplakia(2) Leukoplakia

Mild or Thin Leukoplakia

Homogenous or Thick Leukoplakia

Granular or Nodular Leukoplakia

Verrucous or Verruciform Leukoplakia

(2) Leukoplakia

Proliferative Verrucous Leukoplakia (PVL)

Erythroleukoplakia or Speckled Leukoplakia

(2) Leukoplakia

(2) Leukoplakia

Mild or Thin Leukoplakia

seldom shows dysplasia on biopsy

may disappear or continue unchanged

(2) Leukoplakia

Homogenous or Thick Leukoplakia

for tobacco smokers who do not reduce their habit

2/3 of such lesions slowly extend laterally, become thicker + acquire distinctly white appearance

(2) Leukoplakia

Homogenous or Thick Leukoplakia

affected mucosa may become leathery to palpation

fissures may deepen

become more numerous

most thick, smooth lesions remain indefinitely at this stage

(2) Leukoplakia

Homogenous or Thick Leukoplakia

some, perhaps as many as 1/3, regress or disappear

(2) Leukoplakia

Granular or Nodular Leukoplakia

few become even more severe

develop increased surface irregularities

(2) Leukoplakia

Verrucous or Verruciform Leukoplakia

lesions that demonstrate sharp or blunt projections

(2) Leukoplakia

Proliferative Verrucous Leukoplakia (PVL)

high risk form of leukoplakia

development of multiple keratotic plaques

with roughened surface projections

(2) Leukoplakia

Proliferative Verrucous Leukoplakia (PVL)

tend to slowly spread

involve additional oral mucosal sites

gingiva is frequently involved

although other sites may be affected as well

(2) Leukoplakia

Proliferative Verrucous Leukoplakia (PVL)

as lesions progress, there may go through a stage indistinguishable

transform into full-fledged squamous cell carcinoma (usually within 8 years of initial PVL diagnosis)

(2) Leukoplakia

Proliferative Verrucous Leukoplakia (PVL)

lesions rarely regress despite therapy

strong female predilection

minimal association with tobacco use

(2) Leukoplakia

Erythroplakia

leukoplakia may become dysplastic

even invasive, with no change in its clinical appearance

however, some lesions eventually demonstrate scattered patches of redness called erythroplakia

(2) Leukoplakia

Erythroleukoplakia or Speckled Leukoplakia

such areas usually represent sites in which epithelial cells are so immature or atrophic that they can no longer produce keratin

(2) Leukoplakia

Erythroleukoplakia or Speckled Leukoplakia

intermixed red-and-white lesion

pattern of leukoplakia that frequently reveals advanced dysplasia on biopsy

(2) Leukoplakia

Etiology & Prognosis

many cases are etiologically related to use of tobacco in smoked or smokeless forms and may regress after discontinuation of tobacco use

(2) Leukoplakia

Etiology & Prognosis

other factors, such as • alcohol abuse may have• trauma a role in• C. albicans infection etiology

(2) Leukoplakia

Etiology & Prognosis

nutritional factors have been cited as important, especially iron deficiency anemia

(2) Leukoplakia

Clinical Features

associated with middle-aged + older population

vast majority of cases occur after age of 40 years

(2) Leukoplakia

Site of Occurence

Vestibule Buccal Palate Alveolar Ridge Lip Tongue Floor

(2) Leukoplakia

leukoplakia of lips + tongue also exhibits relative high percentage of dysplastic or neoplastic change

(2) Leukoplakia

Treatment & Prognosis

absence of dysplastic or atypical epithelial changes

• periodic examinations + rebiopsy of new suspicious areas are recommended

(2) Leukoplakia

Treatment & Prognosis

if diagnosis as moderate to severe dysplasia

• excision is obligatory

for large lesions, grafting procedures may be necessary after surgery

may recur after complete removal

(2) Leukoplakia

chronic mucocutaneous disease of unknown cause

relatively common

typically presents as bilateral white lesions

occasionally with associated ulcers

(3) Lichen Planus

Pathogenesis

although cause is unknown

generally considered to be a immunologically mediated process

resembles hypersensitivity reaction

(3) Lichen Planus

Clinical Features

disease of middle age

affects men + women in nearly equal numbers

children rarely affected

(3) Lichen Planus

Clinical Features

Types:

• Reticular• Erosive (ulcerative)• Plaque• Papular • Erythematous (atrophic)

(3) Lichen Planus

Clinical Features

Reticular Form

• most common type

• numerous interlacing white keratotic lines or striae

(Wickham’s striae)

produces anular or lacy pattern

(3) Lichen Planus

Clinical Features

Reticular Form

• buccal mucosa is the site most commonly involved

• may also be noted on:

tongue gingiva – less common lips

(3) Lichen Planus

Clinical Features

Plaque Form

• resembles leukoplakia

• but has multifocal distribution

• range from slightly elevated to smooth and flat

(3) Lichen Planus

Clinical Features

Plaque Form

• primary sites are

dorsum of tongue buccal mucosa

(3) Lichen Planus

Clinical Features

Erythematous Form

• red patches

• with very fine white striae

• attached gingiva commonly involved

(3) Lichen Planus

Clinical Features

Erythematous Form

• patchy distribution often in four quadrants

• patient may complain of

burning sensitivity generalized discomfort

(3) Lichen Planus

Clinical Features

Erosive Form

• central area of lesion is ulcerated

• fibrinous plaque or pseudomembrane covers ulcer

• changing patterns of involvement from week to week

(3) Lichen Planus

Treatment

although it cannot be generally cured

some drugs can provide satisfactory control

corticosteroids are the single most useful group of drugs in the management of lichen planus

(3) Lichen Planus

Treatment

corticosteroid

• ability to modulate inflammation + immune response

(3) Lichen Planus

Treatment

topical application + local injection of steroids have been used successfully in controlling but not curing this disease

(3) Lichen Planus

common oppurtunistic oral mycotic infection

develops in the presence of one of several predisposing factors

• immunodeficiency• endocrine disturbances• hypoparathyroidism• diabetes mellitus• poor oral hygiene • xerostomia

(4) Candidiasis

caused by Candida albicans

infection with this organism is usually superficial, affecting the outer aspects of involved oral mucosa or skin

(4) Candidiasis

in severely debilitated + immunocompromised patients such as patients with AIDS

infection may extend into alimentary tract (candidal esophagitis

bronchopulmonary tract

and other organ system

(4) Candidiasis

Clinical Features

most common form is acute pseudomembranous also known, as thrush

• young infants + elderly are commonly affected

(4) Candidiasis

Clinical Features

oral lesion of acute candidiasis (thrush)

• white• soft plaques that sometime grow centrifugally + merge• wiping plaques with gauze sponge leaves a painful, eroded, eryhtematous or ulcerated surface

(4) Candidiasis

Clinical Features

Chronic Erythematous Candidiasis

• commonly seen on geriatric individuals

• who wear complete maxillary denture

(4) Candidiasis

Clinical Features

Chronic Erythematous Candidiasis

• distinct predilection for palatal mucosa as compared with mandibular alveolar arch

(4) Candidiasis

Clinical Features

Chronic Erythematous Candidiasis

• chronic low-grade resulting from poor prosthesis fit

• failure to remove appliance at night

(4) Candidiasis

Clinical Features

Chronic Erythematous Candidiasis

• bright red

• relative little keratinization

(4) Candidiasis

Clinical Features

Hyperplastic Candidiasis

• may involve dorsum of tongue

• pattern referred to as median rhomboid glossitis

(4) Candidiasis

Clinical Features

Hyperplastic Candidiasis

• usually asymptomatic

• usually discovered on routine oral examination

(4) Candidiasis

Clinical Features

Hyperplastic Candidiasis

• found anterior to circumvallate papillae

• oval or rhomboid outline

(4) Candidiasis

Clinical Features

Hyperplastic Candidiasis

• may have smooth, nodular or fissured surface

• range in color from white to more red

(4) Candidiasis

Clinical Features

Mucocutaneous Candidiasis

• long standing

• persistent candidiasis of

oral mucosa skin vaginal mucosa

(4) Candidiasis

Clinical Features

Mucocutaneous Candidiasis

• often resistant to treatment

• begins as a pseudomembranous type of candidiasis

• soon followed by nail + cutaneous involvement

(4) Candidiasis

Treatment

majority of infections may be simply treated with topical applications of nystatin suspension

• nystatin cream or ointment often effective when applied directly to denture-bearing surface itself

(4) Candidiasis

Treatment

topical applications of either nystatin or clotrimazole should be continued for at least 1 week beyond disappearance of clinical manifestations of disease

(4) Candidiasis

Treatment

Hyperplastic Candidiasis

• topical + systemic antifungal agents may not be effective at completely removing lesions

surgical management may be necessary

(4) Candidiasis

Treatment

Chronic Mucocutaneous Candidiasis associated with immunosuppression

• topical agents may not be effective

(4) Candidiasis

Treatment

Chronic Mucocutaneous Candidiasis associated with immunosuppression

• systemic administration of medications:

Ketoconazole Fluconazole Itraconazole

(4) Candidiasis

autosomal-dominant condition

due to point mutations for genes coding for keratin 4 and/or 13.

affects oral mucosa bilaterally

NO treatment is required

(5) White Sponge Nevus

Clinical Features

• asymptomatic

• folded white lesions

• may affect several mucosal sites

• lesions tend to be thickened + spongy consitency

(5) White Sponge Nevus

Clinical Features

• presentation intraorally is almost always bilateral + symmetric

• usually appears early in life, typically before puberty

(5) White Sponge Nevus

Clinical Features

• usually observed in buccal mucosa

• tongue + vestibular mucosa may be involved

(5) White Sponge Nevus

Treatment

• NO treatment necessary since it is asymptomatic + benign

(5) White Sponge Nevus

common tobacco-related form of keratosis

typically associated with pipe + cigar smoking

with positive correlation between intensity of smoking + severity of condition

(6) Nicotine Stomatitis

combination of tobacco carcinogens + heat is markedly intensified in reverse smoking (lit end positioned inside the mouth)

adding a significant risk for malignant conversion

(6) Nicotine Stomatitis

Clinical Features

palatal mucosa initially responds with an erythematous change follwed by keratinization

(6) Nicotine Stomatitis

Clinical Features

subsequent to opacification or keratinization of palate

• red dots surrounded by white keratotic rings appear

dot represent inflammation of salivary gland excretory duct

(6) Nicotine Stomatitis

Treatment

condition rarely evolves into malignancy

except in individuals who reverse smoke

discontinuation of tobacco habit

(6) Nicotine Stomatitis

also known as erythema migrans, benign migratory glossitis

prevalent among whites + blacks

strongly associated with fissure tongue

inversely associated with cigarette smoking

(7) Geographic Tongue

emotional stress may enhance the process

(7) Geographic Tongue

Clinical Features

affects women slightly more than men

children occasionally may be affected

characterized initially by presence of atrophic patches surrounded by elevated keratotic margins

(7) Geographic Tongue

Clinical Features

desquamated areas appear red + may be slightly tender

followed over a period of days or weeks, pattern changes

appearing to move across dorsum of tongue

(7) Geographic Tongue

Clinical Features

most patients are asymptomatic

occasionally patients complain of irritation or tenderness

especially in relation to consumption of spicy foods + alcoholic beverages

(7) Geographic Tongue

Clinical Features

lesions periodically disappear

recur for no apparent reason

(7) Geographic Tongue

Treatment

NO treatment is required because of self-limiting + usually asymptomatic nature of this condition

(7) Geographic Tongue

Treatment

when symptoms occur,

• topical steroids especially ones containing antifungal agent

helpful in reducing symptoms

(7) Geographic Tongue

Treatment

mouth clean using mouthrinse composed of sodium bicarbonate in water

reassure patients that condition is totally benign

(7) Geographic Tongue

clinical term referring to a condition of filiform papillae overgrowth on dorsal surface of tongue

there are numerous initiating or predisposing factors for hairy tongue

(8) Hairy Tongue

broad spectrum antibiotics such as penicillin + systemic cortiocosteroids are often identified in clinical history of patients with this condition

(8) Hairy Tongue

oxygenating mouthrinses containing:

hydrogen peroxide sodium perborate carbamide peroxide

have been cited as possible etiologic agents

(8) Hairy Tongue

Clinical Features

clinical alteration translates to hyperplasia of filiform papillae; result is

• thick serves to trap• matted surface bacteria, fungi, foreign materials

(8) Hairy Tongue

Clinical Features

extensive elongation of papillae occurs,

• gagging may be• tickiling sensation felt

(8) Hairy Tongue

Clinical Features

color may range from white to tan to deep brown depending on:

• diet• oral hygiene• composition of bacteria inhabiting papillary surface

(8) Hairy Tongue

Treatment

brush/scrape tongue with baking soda

maintain good oral hygiene

emphasize to patients that this process is entirely benign

(8) Hairy Tongue

Treatment

self-limiting

tongue should return to normal after institution of physical debridement + proper oral hygiene

(8) Hairy Tongue

also known as Gingival Cyst of New Born or Bohn’s nodules

appear as multiple nodules along alveolar ridge in neonates

(9) Dental Lamina Cyst

similar epithelial inclusion cysts may occur along midline of palate (palatine cyst of new born or Epstein’s pearls)

developmental origin derived from epithelium included in fusion line between palatal shelves + nasal processes no treatment; resolve spontaneously

(9) Dental Lamina Cyst

Treatment

not necessary because nearly all spontaneously rupture before patient is 3 months of age

(9) Dental Lamina Cyst

represents ectopic sebaceous glands or sebaceous choristomas

normal tissue in abnormal location

regarded as developmental

considered a variation of normal

(10) Fordyce’s Granules

multiple

often seen in aggregates

sites of predilection include

• buccal mucosa• vermillion of upper lip

(10) Fordyce’s Granules

lesions generally are symmetrical distributed

tend to become obvious after puberty

maximal expression occurring between 20-30 years of age

(10) Fordyce’s Granules

lesions are asymptomatic

discovered during routine oral examination

(10) Fordyce’s Granules

Treatment

No treatment is indicated

• glands are normal in character

• do not cause any untoward effects

(10) Fordyce’s Granules

also known as Angular Cheilitis

inflammation + atrophy of skin of folds at angles of mouth

(11) Perleche

may be due to:

excessive lip licking

thumb sucking

sagging of facial skin in edentulous or elderly persons

(11) Perleche

may be due to:

prolonged contact with saliva results in maceration with possible secondary infection by Candida or staphylococci

(11) Perleche

Clinical Features

skin at angles of mouth has erythematous fissures

often with exudate + crust

further licking to moisten inflamed area exacerbates the problem

(11) Perleche

Treatment

applying antimicrobial creams

followed by low-potency steroid creams until symptoms resolve

protective lip balm may help prevent recurrence

(11) Perleche

References:References:

BooksBooks

Cawson, R.A: Cawson’s Essentials of OralCawson, R.A: Cawson’s Essentials of Oral Oral Pathology and Oral Medicine,Oral Pathology and Oral Medicine, 88thth Edition Edition

• (page 165-167 )(page 165-167 ) Neville, et. al: Oral and Maxillofacial PathologyNeville, et. al: Oral and Maxillofacial Pathology 33rdrd Edition Edition

• (pages 388- 397; 590-592; 819-820) (pages 388- 397; 590-592; 819-820) Regezi, et. al: Oral Pathology: Clinical PathologicRegezi, et. al: Oral Pathology: Clinical Pathologic Correlations, 5Correlations, 5thth Edition Edition

• (pages 73-105; 241-242; 296-299; 394)(pages 73-105; 241-242; 296-299; 394)

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