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WHITE LESIONS Prepared by: Dr. Rea Corpuz

White lesions (2)

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Page 1: White lesions (2)

WHITE LESIONS

Prepared by:Dr. Rea Corpuz

Page 2: White lesions (2)

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

Page 3: White lesions (2)

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

ulcer submucosal deposit surface debris fungal colonies

White Lesions

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(1) Leukoedema

(2) Leukoplakia

(3) Lichen Planus

(4) Candidiasis

(5) White Sponge Nevus

(6) Nicotine Stomatitis

White Lesions

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(7) Geographic Tongue

(8) Hairy Tongue

(9) Dental Lamina Cyst

(10) Fordyce’s Disease

(11) Perleche

White Lesions

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

can be identified in majority of population

(1) Leukoedema

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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

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Clinical Features

usual discovered as incidental finding

asymptomatic

symmetrically distributed in buccal mucosa

(1) Leukoedema

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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

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Clinical Features

with stretching of buccal mucosa, opaque changes dissipate

more apparent in non-whites, especially African-American

(1) Leukoedema

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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

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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

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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

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Mild or Thin Leukoplakia

Homogenous or Thick Leukoplakia

Granular or Nodular Leukoplakia

Verrucous or Verruciform Leukoplakia

(2) Leukoplakia

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Proliferative Verrucous Leukoplakia (PVL)

Erythroleukoplakia or Speckled Leukoplakia

(2) Leukoplakia

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(2) Leukoplakia

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Mild or Thin Leukoplakia

seldom shows dysplasia on biopsy

may disappear or continue unchanged

(2) Leukoplakia

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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

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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

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Homogenous or Thick Leukoplakia

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

(2) Leukoplakia

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Granular or Nodular Leukoplakia

few become even more severe

develop increased surface irregularities

(2) Leukoplakia

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Verrucous or Verruciform Leukoplakia

lesions that demonstrate sharp or blunt projections

(2) Leukoplakia

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Proliferative Verrucous Leukoplakia (PVL)

high risk form of leukoplakia

development of multiple keratotic plaques

with roughened surface projections

(2) Leukoplakia

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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

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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

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Proliferative Verrucous Leukoplakia (PVL)

lesions rarely regress despite therapy

strong female predilection

minimal association with tobacco use

(2) Leukoplakia

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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

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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

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Erythroleukoplakia or Speckled Leukoplakia

intermixed red-and-white lesion

pattern of leukoplakia that frequently reveals advanced dysplasia on biopsy

(2) Leukoplakia

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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

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Etiology & Prognosis

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

(2) Leukoplakia

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Etiology & Prognosis

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

(2) Leukoplakia

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Clinical Features

associated with middle-aged + older population

vast majority of cases occur after age of 40 years

(2) Leukoplakia

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Site of Occurence

Vestibule Buccal Palate Alveolar Ridge Lip Tongue Floor

(2) Leukoplakia

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

(2) Leukoplakia

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Treatment & Prognosis

absence of dysplastic or atypical epithelial changes

• periodic examinations + rebiopsy of new suspicious areas are recommended

(2) Leukoplakia

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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

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chronic mucocutaneous disease of unknown cause

relatively common

typically presents as bilateral white lesions

occasionally with associated ulcers

(3) Lichen Planus

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Pathogenesis

although cause is unknown

generally considered to be a immunologically mediated process

resembles hypersensitivity reaction

(3) Lichen Planus

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Clinical Features

disease of middle age

affects men + women in nearly equal numbers

children rarely affected

(3) Lichen Planus

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Clinical Features

Types:

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

(3) Lichen Planus

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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

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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

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Clinical Features

Plaque Form

• resembles leukoplakia

• but has multifocal distribution

• range from slightly elevated to smooth and flat

(3) Lichen Planus

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Clinical Features

Plaque Form

• primary sites are

dorsum of tongue buccal mucosa

(3) Lichen Planus

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Clinical Features

Erythematous Form

• red patches

• with very fine white striae

• attached gingiva commonly involved

(3) Lichen Planus

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Clinical Features

Erythematous Form

• patchy distribution often in four quadrants

• patient may complain of

burning sensitivity generalized discomfort

(3) Lichen Planus

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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

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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

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Treatment

corticosteroid

• ability to modulate inflammation + immune response

(3) Lichen Planus

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Treatment

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

(3) Lichen Planus

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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

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caused by Candida albicans

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

(4) Candidiasis

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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

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Clinical Features

most common form is acute pseudomembranous also known, as thrush

• young infants + elderly are commonly affected

(4) Candidiasis

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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

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Clinical Features

Chronic Erythematous Candidiasis

• commonly seen on geriatric individuals

• who wear complete maxillary denture

(4) Candidiasis

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Clinical Features

Chronic Erythematous Candidiasis

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

(4) Candidiasis

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Clinical Features

Chronic Erythematous Candidiasis

• chronic low-grade resulting from poor prosthesis fit

• failure to remove appliance at night

(4) Candidiasis

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Clinical Features

Chronic Erythematous Candidiasis

• bright red

• relative little keratinization

(4) Candidiasis

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Clinical Features

Hyperplastic Candidiasis

• may involve dorsum of tongue

• pattern referred to as median rhomboid glossitis

(4) Candidiasis

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Clinical Features

Hyperplastic Candidiasis

• usually asymptomatic

• usually discovered on routine oral examination

(4) Candidiasis

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Clinical Features

Hyperplastic Candidiasis

• found anterior to circumvallate papillae

• oval or rhomboid outline

(4) Candidiasis

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Clinical Features

Hyperplastic Candidiasis

• may have smooth, nodular or fissured surface

• range in color from white to more red

(4) Candidiasis

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Clinical Features

Mucocutaneous Candidiasis

• long standing

• persistent candidiasis of

oral mucosa skin vaginal mucosa

(4) Candidiasis

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Clinical Features

Mucocutaneous Candidiasis

• often resistant to treatment

• begins as a pseudomembranous type of candidiasis

• soon followed by nail + cutaneous involvement

(4) Candidiasis

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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

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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

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Treatment

Hyperplastic Candidiasis

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

surgical management may be necessary

(4) Candidiasis

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Treatment

Chronic Mucocutaneous Candidiasis associated with immunosuppression

• topical agents may not be effective

(4) Candidiasis

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Treatment

Chronic Mucocutaneous Candidiasis associated with immunosuppression

• systemic administration of medications:

Ketoconazole Fluconazole Itraconazole

(4) Candidiasis

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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

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Clinical Features

• asymptomatic

• folded white lesions

• may affect several mucosal sites

• lesions tend to be thickened + spongy consitency

(5) White Sponge Nevus

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Clinical Features

• presentation intraorally is almost always bilateral + symmetric

• usually appears early in life, typically before puberty

(5) White Sponge Nevus

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Clinical Features

• usually observed in buccal mucosa

• tongue + vestibular mucosa may be involved

(5) White Sponge Nevus

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Treatment

• NO treatment necessary since it is asymptomatic + benign

(5) White Sponge Nevus

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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

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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

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Clinical Features

palatal mucosa initially responds with an erythematous change follwed by keratinization

(6) Nicotine Stomatitis

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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

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Treatment

condition rarely evolves into malignancy

except in individuals who reverse smoke

discontinuation of tobacco habit

(6) Nicotine Stomatitis

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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

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emotional stress may enhance the process

(7) Geographic Tongue

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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

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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

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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

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Clinical Features

lesions periodically disappear

recur for no apparent reason

(7) Geographic Tongue

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Treatment

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

(7) Geographic Tongue

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Treatment

when symptoms occur,

• topical steroids especially ones containing antifungal agent

helpful in reducing symptoms

(7) Geographic Tongue

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Treatment

mouth clean using mouthrinse composed of sodium bicarbonate in water

reassure patients that condition is totally benign

(7) Geographic Tongue

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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

Page 92: White lesions (2)

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

(8) Hairy Tongue

Page 93: White lesions (2)

oxygenating mouthrinses containing:

hydrogen peroxide sodium perborate carbamide peroxide

have been cited as possible etiologic agents

(8) Hairy Tongue

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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

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Clinical Features

extensive elongation of papillae occurs,

• gagging may be• tickiling sensation felt

(8) Hairy Tongue

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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

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Treatment

brush/scrape tongue with baking soda

maintain good oral hygiene

emphasize to patients that this process is entirely benign

(8) Hairy Tongue

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Treatment

self-limiting

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

(8) Hairy Tongue

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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

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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

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Treatment

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

(9) Dental Lamina Cyst

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represents ectopic sebaceous glands or sebaceous choristomas

normal tissue in abnormal location

regarded as developmental

considered a variation of normal

(10) Fordyce’s Granules

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multiple

often seen in aggregates

sites of predilection include

• buccal mucosa• vermillion of upper lip

(10) Fordyce’s Granules

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lesions generally are symmetrical distributed

tend to become obvious after puberty

maximal expression occurring between 20-30 years of age

(10) Fordyce’s Granules

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lesions are asymptomatic

discovered during routine oral examination

(10) Fordyce’s Granules

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Treatment

No treatment is indicated

• glands are normal in character

• do not cause any untoward effects

(10) Fordyce’s Granules

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also known as Angular Cheilitis

inflammation + atrophy of skin of folds at angles of mouth

(11) Perleche

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may be due to:

excessive lip licking

thumb sucking

sagging of facial skin in edentulous or elderly persons

(11) Perleche

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may be due to:

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

(11) Perleche

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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

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Treatment

applying antimicrobial creams

followed by low-potency steroid creams until symptoms resolve

protective lip balm may help prevent recurrence

(11) Perleche

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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)