d of keratotic white lesions

DIFFERENTIAL DIAGNOSIS OF KERATOTIC WHITE

LESION

presented by :-

Y.PRIYANKA RAO

1Saturday 11 June 2011

INTRODUCTION.

CLASSIFICATION.

DIFFERENTIAL DIAGNOSIS OF KERATOTIC WHITE LESIONS.

CONCLUSION.

REFERENCES.


DEFINITION:-

Any condition that increases the thickness of the epithelium causes it to appear white by increasing the distance to the vascular bed.

CAUSES:-

it is due to the hyperkeratosis ; any excess keratin , becoming sodden with saliva appears white.

hyperplasia of epithelium.

marked intracellular edema.

much microvesicular formation in the prickle cell layer.

INTRODUCTION


CLASSIFICATION :-A) keratotic white lesions :-

1) HEREDITARY WHITE LESIONS:-white sponge nevus.

leukoedema.hereditary benign intraepithelial dyskeratosis.

dyskeratosis congenita.2) REACTIVE/INFLAMMATORY WHITE LESIONS:-

linea alba(white line).FOCAL (frictional) keratosis & cheek biting.

smokeless tobacco-induced keratosis.nicotine stomatitis.

3) INFECTIOUS WHITE LESIONS:-oral hairy leukoplakia.

mucous patches.Candidiasis.

4) LICHEN PLANUS.5) DRUG INDUCED LICHENOID REACTIONS.6) SKIN GRAFT.7) LUPUS ERYTHEMATOSUS.8) LEUKOPLAKIA.9) MISCELLANEOUS LESIONS:-

benign migratory glossitis & mucositis.4Saturday 11 June 2011

HEREDITARY WHITE LESION

KERATOTIC WHITE LESIONS

WHITE SPONGE NEVUS


white sponge nevus:-(familial white folded gingivostomatitis)

ETIOLOGY:-1) It is a developmental anomaly .

2) Inherited as an autosomal dominant trait , caused by mutation in keratin genes.

CLINICAL FEATURES:-1)Affected mucosa is white,soft & irregularly thickened

white folded appearance.

2)Usually bilateral.

3)No defined borders.

4)Edges fade imperceptibly into normal tissue.


WHITE SPONGE NEVUS


Leukoedema:- It is only opalescent & white sponge has rough granular & lethargic appearance.

Leukoplakia:- It occurs over 40 years of age & not disseminated throughout the oral cavity. white sponge nevus occur soon after birth or atleast by puberty & widely distributed over the oral mucous membrane.

Hereditary benign intraepithelial dyskeratosis:- Involves buccal, labial mucosa,lateral tongue , floor of the mouth,the gingiva & palate ,along with conjuctiva . Occular lesions manifest during the first year of life.

Pachyonychia congentia:- Presence of nail anomalies as well as skin lesions.

differential diagnosis:-


LEUKOEDEMA.


LEUKOEDEMAETIOLOGY:- USE OF TOBACCO.

PH OF SALIVA.ORAL BACTERIAL INFECTION.

SYPHILIS OR GALVANIC IRRITATION.

CLINICAL FEATURES :-

1) ASYMPTOMATIC

2) FREQUENTLY ON BUCCAL MUCOSA , LABIAL MUCOSA & SOFT PALATE.

3) BILATERAL , DIFFUSE , TRANSLUCENT GRAYISH-WHITE THICKENING.

4) IT DISAPPEARS OR FADES UPON STRETCHING THE MUCOSA.


LEUKOEDEMA

Leukoedema with a faint white diffuse filmy appearanceand mild wrinkling of the mucosa.


DIFFERENTIAL DIAGNOSIS:-1 )LEUKOPLAKIA:- A) LEUKOEDEMA HAS FAINT MILKY APPEARANCE, FOLDED & WRINKLED PATTERN AS COMPARED TO DEFINITE WHITENESS OF LEUKOPLAKIA.B) CANNOT ELIMINATE BY STRETCHING.

2 )CHEEK BITING LESION:- A) FOUND BILATERALLY ON POSTERIOR BUCCAL MUCOSA ALONG THE PLANE OF OCCLUSION. B) ASSOCIATED WITH TRAUMA.C) ROUGHNESS OR SMALL TAGS OF TISSUE THAT THEY ACTUALLY TEAR FREE FROM THE SURFACE.

3) WHITE SPONGE NEVUS:- A) LEUKOEDEMA IS A FAINT , WHITE, DIFFUSE ,FILMY APPEARANCE AND MILD WRINKLES OF MUCOSA. B) FADES OFF ON STRETCHING OF THE MUCOSA.C) WHERE AS WSN DOESNT FADES OFF ON STRETCHING .

4) DYSKERATOSIS HEREDITARY BENIGN INTRAEPITHELIAL:- A) SAME AS WSN .B) IT HAS TYPICAL MICROSCOPIC FEATURE.


REACTIVE/INFLAMMATORY WHITE LESION

FRICTIONAL (TRAUMATIC) KERATOSIS & CHEEK BITING.


FRICTIONAL(traumatic)KERATOSIS & CHEEK BITING:-

ETIOLOGY:-1)prolonged mild abrasion of the mucous membrane such as ;

a)irritant due to sharp cusp & edges of broken tooth. b) cheek biting (or) maladjusted dentures.

Definition:- defined as “ a white plaque with rough & frayed surface that is clearly related to an identifiable source of mechanical irritation that will usually resolve on elimination of the irritant.”

SITES:- Most common sites are lip and buccal mucosa.

APPEARANCE:- At first appears;pale and translucent , later become dense and white.

CLINICAL FEATURES:-


CHEEK BITING

DIFFERENTIAL DIAGNOSIS:-

Sometimes mimic dysplastic leukoplakia.

Isolated white patch with identified local irritant.


LINEA ALBA.16Saturday 11 June 2011

LINEA ALBA:-“A horizontal streak on the buccal mucosa at the level of occlusal plane extending from the commissure to the posterior teeth.”

ETIOLOGY:-Associated with pressure ,frictional irritation , or sucking trauma from the facial surfaces of the teeth.

Usually present bilaterally.

More prominent in individuals with reduced overjet of the posterior teeth.

often scalloped and restricted to dentulous areas.

CLINICAL FEATURES:-


A HORIZONTAL STREAK AT THE LEVEL OCCLUSAL

PLANE.

LINEA ALBA:-


smokeless tobacco-induced keratosis.


smokeless tobacco-induced keratosis.

CLINICAL FEATURES:-Development of root surface caries .

Increased amount of gingival recession with periodontal destruction in the immediate area of contact.

The most common area of involvement is the anterior mandibular vestibule

followed by the posterior vestibule.

Surface of the mucosa appears gray or gray-white & is granular, wrinkled & translucent.

stretched mucosa appears fissured or rippled & a “pouch” is usually present.

The white pouch may become leathery or nodular in long term heavy users.

Habitually chewing tobacco leaves or dipping snuff results in the

development of a well-recognized white mucosal lesion in the area of tobacco contact, called smokeless tobacco keratosis,snuff dipper’s keratosis, or tobacco pouch keratosis


White leathery nodular tobacco pouch Snuff pouch with a white wrinkled mucosal surface.

Differential Diagnosis• Leukoplakia (idiopathic)• Mucosal burn (chemical/thermal)

Snuff pouch showing extensive periodontal tissue

destruction and a thickened area of leukoplakia.


NICOTINE STOMATITIS.


NICOTINE STOMATITISA specific white lesion that develops on the hard and soft palate in heavy cigarette, pipe, and cigar smokers.

The palatal mucosa becomes diffusely gray or white.

Numerous slightly elevated papules with punctate red centers that represent inflamed & metaplastically altered minor salivary gland ducts are noted.

CLINICAL FEATURES:-

Nicotine stomatitis with diffuse white change in thepalatal mucosa, along with elevated papules with red centers.


INFECTIOUS WHITE LESIONS.


ORAL HAIRY LEUKOPLAKIA


Oral hairy leukoplakia is a corrugated white lesion that usually occurs on the lateral or ventral surfaces of the tongue in patients with severe immunodeficiency.

ETIOLOGY:-

ORAL HAIRY LEUKOPLAKIA:-

1)The most common disease associated with oral hairy leukoplakia is HIV infection.

2)Epstein-Barr virus (EBV) is implicated as the causative agent in oral hairy leukoplakia.

CLINICAL FEATURES:-1)Oral hairy leukoplakia most commonly involves the lateral border of the tongue but may extend to the ventral or dorsal surfaces.

2)Usually corrugated and may have a shaggy or frayed appearance, mimicking lesions caused by tongue chewing.

3)It may also present as a plaquelike lesion and is often bilateral.


Typical white corrugated leukoplakia in the maxillary vestibule, associated with sanguinaria use.

Mandibular vestibular lesion

Bilateral linear leukoplakic lesions on the dorsolateral tongue, suggestive of oral hairy leukoplakia.



1)It is important to differentiate this lesion from other clinically similar entities such as Hyperplastic candidiasis:- These patients develop similar lesions around the nails and other skin sites or alternatively develop only isolated oral lesions. lichen planus.lupus erythematosus.WSN .idiopathic leukoplakia.

2)Since oral hairy leukoplakia is considered to be highly predictive of the development of AIDS, differentiation from other lesions is critical.


Classification of Oral Candidiasis:-Acute

PseudomembranousAtrophic (erythematous)

Antibiotic stomatitis

ChronicAtrophic

Denture sore mouthAngular cheilitis

Median rhomboid glossitisHypertrophic/hyperplastic

Candidal leukoplakiaPapillary hyperplasia of the palate (see denture sore mouth)

Median rhomboid glossitis (nodular)Multifocal

MucocutaneousSyndrome associated

Familial +/– endocrine candidiasis syndromeMyositis (thymoma associated)

LocalizedGeneralized (diffuse)

Immunocompromise (HIV) associated

CANDIDIASIS:-


1)Candidiasis is the most common oral fungal infectioncaused by candida albicans.

2) Associated with predisposing factors: most commonly, immunosuppression, diabetes mellitus, antibiotic use, or xerostomia (due to lack of protective effects of saliva).

1)The pseudomembranous andhyperplastic type of candidiasis present as white lesions of

the oral cavity. 2)Pseudomembranous candidiasis, also

known as thrush is characterized by adherent white plaques resembling curdled milk.

3) Scraping the white lesion can remove the plaques. 4)The hyperplastic candidiasis or candidal leukoplakia

presents as non-scrapable white patch usually located on the anterior buccal mucosa .

1)Hyperplastic candidiasis cannot be clinically distinguished from leukoplakia.

2)The diagnosis is confirmed by the presence of candidal hyphae in the lesions and resolution of the lesion after

antifungal therapy.

ETIOLOGY:-

CLINICAL FEATURES:-


pseudomembranous candidiasis.

hyperplastic candidiasis:-


ORAL LICHEN PLANUS


“Oral lichen planus (OLP) is a common chronic immunologic inflammatory mucocutaneous disorder that varies in appearance from keratotic (reticular or plaquelike) to erythematous and ulcerative.”

The etiology of lichen planus involves a cell-mediated immunologically induced degeneration of the basal cell layer of the epithelium.

Clinical and microscopic changes that are consistent with OLP will often occur in response to a variety of agents (eg, drugs, chemicals, metals, and foods).When these manifestations take place, they arereferred to as “lichenoid” reactions.

ORAL LICHEN PLANUS

Etiology:-

Reticular lichen planus of the buccal mucosa.


The fifth decade of life.

A female predominance.

The buccal mucosa is the most common site.

OLP is classified as :- 1) reticular (lacelike keratotic mucosal configurations),

2)atrophic (keratotic changes combined with mucosal erythema), 3) erosive (pseudomembrane-covered ulcerations combined with keratosis and erythema) .

4) bullous (vesiculobullous presentation combined with reticular or erosive

Reticular form consists of slightly elevated fine whitish lines (Wickham’s striae) that produce either a lacelike pattern or a patern of fine radiating lines or annular lesions.

This is the most common and most readily recognized form of lichen planus patterns.

Whitish elevated lesions, or papules, usually measuring 0.5 to 1.0 mm in diameter, may be seen on the well-keratinized areas of the oral mucosa

Clinical features:-


Bullous lichen planus is rare .

Atrophic lichen planus presents as inflamed areas of the oral mucosacovered by thinned red-appearing epithelium.

Erosive lesions probably develop as a complication of the atrophic processwhen the thin epithelium is abraded or ulcerated.

Papular, plaquelike, atrophic, and erosive lesions are very frequently accompanied by reticular lesions.

The keratotic white lines cannot be eliminated by either stretching the mucosa or rubbing.

Atrophic, erosive, and bullous forms are generally associated with pain.

Erosive lichen planus of the tongue.

Atrophic lichen planus of the gingiva.


Verruciform leukoplakia:-The surface is excessively keratinized by parakeratin, orthokeratin, or a combination . On mucosal surfaces which are normally heavily keratinized, this keratin hyperplasia may represent more than half of the entire epithelial thickness and may show short, pointed surface projections .

Discoid and systemic lupus erythematosus :- May present with oral keratotic and ulcerative lesions which are clinically identical to lichen planus .Have broader dimension.Flaky & feathery appearance of lupus lesion.

Candidiasis:- Pseudomembrane can be rubbed off in case of candidiasis.

Pemphigus:- Characteristic white striation of lichen planus are usually evident.the absence of immunoglobulin or complement reactivity, to rule out other autoimmune disorders such as pemphigoid and lupus erythematosus.

Graft-vs-host disease:- The lymphocytic band in GVHD is usually more sparse and less well-defined than that of idiopathic lichen planus, and marked fibrosis of subepithelial stroma is common in long-standing cases. Subepithelial blistering is rare except during acute stage disease, in which case skin involvement is quite likely and greatly aids in the diagnosis.



LEUKOPLAKIALeukoplakia is a white oral precancerous lesion with a recognizable risk for malignant transformation.DEFINITION:- “A predominantly white lesion of oral mucosa that cannot be characterized as any other definable lesion.”

Hyperkeratosis of the palate in a heavy pipe smokerappears as an area of leukoplakia

ETIOLOGYTOBACCO.ALCOHOL.

SANGUINARIA.ULTRAVIOLET RADIATION.

MICRO-ORGANISMS.TRAUMA .


CLINICAL FEATURES:-occurs in adults older than 50 years of age.

Leukoplakia lesions are found on the buccal mucosa, vermilion border of the lower lip, and gingiva & tongue.SUBTYPES:-Mild lesions appear slightly elevated gray -white plaques.

Thicker lesions (homogenous) extend laterally & becomes leathery & fissures deepen & appear distinctly white.

Granular or nodular leukoplakia-increase surface irregularities.

Verrucous or verruciform leukoplakia- sharp/blunt projections.

Proliferative verrucous leukoplakia- characteristically ,development of multiple keratotic plaques with roughened surface projections.

Buccal leukoplakia and an adjacent verrucous carcinoma.


Proliferative verrucous leukoplakia of the floor of themouth and of the lip. In this form of leukoplakia, the risk for malignant transformation is very high.

Thick white plaque on the lateral border of tongue representsverrucous leukoplakia. The small ulcerated lesion anterior to the white bumpy lesion is a squamous cell carcinoma


DIFFERENTIAL DIAGNOSIS:-LICHEN PLANUS :- OFTEN OCCURRENCE OF MULTIPLE LESIONS & PRESENCE OF WICKHAM’S STRIAE.

SYPHILITIC MUCUS PATCHES:- FEATURES LIKE SPLIT PAPULE OR CONDYLOMA LATUM MAY BE PRESENT.

WHITE SPONGE NEVUS:- OCCURS SOON AFTER BIRTH OR ATLEAST PUBERTY.WIDELY DISTRIBUTED OVER THE ORAL MUCOUS MEMBRANE.

DISCOID LUPUS ERYTHEMATOUS:- CENTRAL ATROPHIC AREA WITH SMALL WHITE DOT AND SLIGHTLY ELEVATED BORDER ZONE OR RADIATIING WHITE STRIAE.

HAIRY LEUKOPLAKIA:- CORRUGATED LEUKOPLAKIC LESION OCCURS LATERALLY AND VENTRAL SURFACE OF TONGUE .

CHEEK BITING:- CAREFUL HISTORY ELICITS THE CAUSE AND PROMOTES PROPER DIAGNOSIS.

NICOTINE STOMATITIS:- WHITE PALATAL ALTERATIONS,HYPERPLASTIC RESPONSE TO THE HEAT GENERATED BY TOBACCO SMOKING.


CONCLUSION:-

1) White lesions of the oral cavity can range from geneticdisorders like white spongy nevus to potentially malignant

disorders like leukoplakia.

2) Differentiating these lesions histologically are extremely important as the treatment and prognosis

is highly variable.


REFERENCES:-

1) WOOD & GAOZ.

2) SHAFERS.

3) NEVILLE.

4) CAWSON.

5) INTERNET PICTURES.


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