WHITE LESIONS

Prepared by: Dr. Intisar Ben Amer

WHITE LESIONS

The color of the normal oral mucosa is derived from :  Vascularity  Melanin pigmentation  Epithelial thickness  Keratinization

WHITE LESIONS

Any alteration in one of these factors causes discoloration of oral mucosa where:

 Brownish in color indicating excess melanin  Bluish in color indicating vascular lesion  Yellowish in color indicating jaundice

WHITE LESIONS

 Group of pathological conditions affecting oral mucosa gives clinically grayish or white lesions

Microscopical appearance of white lesions

All white lesions are microscopically similar showing 2 main features:  Abnormal keratinization  Increase in the thickness of epithelium through hyperplasia or hypertrophy of the epithelium.

 Hyperkeratosis Increase in the keratin thickness  Hyperorthokeratinization Excessive formation of keratin appearing as flattened cells with no nuclei,Usually there is a granular cell layer below the keratinous layer.  Hyperparakeratinization Excessive formation of keratin with flattened cells containing persistent degenerative nuclei in the superficial cells . There is no granular cell layer

 Keratosis: Keratinization of epithelium that is not normally keratinized.  Acanthosis : increased thickness of prickle cell layer due to increased number of prickle cells.  Hyperplasia : it is increase in the size of a part due to increase in number of cells.  Hypertrophy : It is increase in the size of a part due to increase in the size of the cells.  Atrophy : It is decrease of the epithelial thickness .

ETIOLOGICAL CLASSIFICATION OF WHITE LESIONS OF ORAL MUCOSA

 Hereditary conditions a. Leukodema b. White spongy nevus  Reactive (Traumatic) a. Mechanical (Frictional keratosis) b .Chemical c. Thermal  Infective a. Candidiasis b. Hairy leukoplakia

ETIOLOGICAL CLASSIFICATION OF WHITE LESIONS OF ORAL MUCOSA

 Dermatological a. Lichen planus b. Lupus erythematosis

 Idiopathic Idiopathic leukoplakia

 Neoplastic Squamous cell carcinoma Squamous cell papilloma

I. HEREDITARY CONDITIONS

A) Leukodema

 Definition It is racial pigmention of the buccal mucosa

CLINICAL FEATURES (ASYMPTOMATIC)

 Race: Black women (American, African)  Color: milky whiteness or grayish white area on the surface of mucosa  Appearance: Slightly folded appearance (wrinkled or corrugated )  Consistency: Soft  Site: Buccal mucosa  Diagnosis: The white appearance greatly disappears or diminishes when the cheek is stretched It is now considered as normal variation of OM

HISTOLOGICALLY

 Intracellular edema of prickle cells or spongiosis i.e. increased thickness of prickle cells due to edema  Epithelium is thicker than normal with parakeratinization and acanthosis.  The enlarged epithelial cells have small, pyknotic nuclei in clear cytoplasm.

DIFFERENTIAL DIAGNOSIS

 Leukoplakia  White sponge nevus  Habitual cheek biting

They may show clinical similarity to Leukodema , but they all persist on Stretching the mucosa.

B) WHITE SPONGE NEVUS

 It is an autosomal dominant hereditary disorder that may affect different mucosal sites.

CLINICAL FEATURES: ASYMPTOMATIC

 Age : Infancy or early childhood  Size :It starts small then increase in size to reach its maximum size at the age of adolescence  Appearance : Mucosa appears thickened folded, soft ,white patch with sponge consistency  Site :almost always bilateral and symmetric  Oral lesions : cheeks, palate, gingiva; floor of the mouth, alveolar mucosa & portions of the tongue  Other mucosal lesions : vagina & nasal cavity may be involved

MICROSCOPICALLY

The epithelium is greatly thickened and is showing  Acanthosis  Spongiosis (intracellular edema)  Shaggy Hyperparakeratosis  Cells are edematous , swollen and show prominent cell membrane producing a basket weave appearance which is a characteristic feature of white sponge nevus WHITE SPONGE NEVUS WHITE SPONGE NEVUS

TREATMENT

The disease is benign and has no treatment Reassurance of the patient is all that is needed

II. REACTIVE LESIONS (TRAUMATIC)

A) Mechanical trauma  Frictional keratosis is a white patch caused by prolonged mild irritation of mucous membrane . Acute trauma causes ulcers Long standing chronic trauma causes hyperkeratosis Causes: Irritants such as  Habitual cheek biting (Linea alba)  Orthodontic appliance  Prosthodontic appliance (Ill fitting dentures)  Broken tooth  Rough edges of a carious tooth  Mal aligned teeth

Linea alba

Frictional keratosis FRICTIONAL KERATOSIS

Cheek chewing

HISTOLOGICALLY

 Thick hyperkeratosis with a prominent granular cell layer (hyperorthokeratosis)  No dysplasia  Moderate epithelial hyperplasia , and acanthosis  Some chronic inflammatory cells infiltration in the underlying connective tissue stroma

FRICTIONAL KERATOSIS FRICTIONAL KERATOSIS TREATMENT

Remove causative factor The lesion resolves when source of irritation is removed

B) CHEMICAL

1. Aspirin burn Aspirin tablets are used mistakenly as a local analgesic for the relief of toothache. It is placed against the offending tooth allowing the cheek or lip to hold it in position and to let it dissolve slowly. This causes a burn as aspirin contains acetyl salicylic acid. This produces epithelial sloughing ,necrosis and ulceration. Low grade chronic insult results in hyperkeratosis

B) CHEMICAL

2. Acid etch Causes sometimes Chemical burn 3. Smokeless tobacco  The habit of chewing the tobacco leaves (betel nut)Or holding finely ground tabacco leaves (snuff)in the mandibular vestibule is considered as chronic chemical insult .these habits produce white lesions duo to epithelial thickening and hyperkeratosis.

 Mild absorption of this irritant material through oral mucosa may lead to carcinoma Aspirin burn, creating a pseudomembranous necrotic white area.

Severe ulceration and sloughing of mucosa, caused by use of a cinnamon- containing dentifrice CHEMICAL INJURIES SMOKELESS TOBACCO

C) THERMAL

1. Pizza burn Acute thermal trauma causing a grayish white lesion due to necrotic epithelium surrounded by erythema

2. Smoking induced keratosis Regular smokers of cigarettes, cigars & pipes often develop white lesion on their oral mucosa particularly the anterior parts of buccal mucosa, tongue and palate.

Smokers who constantly dangle a cigarette from lips may develop a localized keratosis at that site. Two factors causes the lesion :  Fumes generated causing hyperkeratinization  Chemicals in fumes (nicotine & tar) are carcinogenic

3. Nicotinic stomatitis Nicotinic stomatitis is a specific white lesion of palate in pipe and cigar smokers.

CLINICALLY

 Palate develops a diffuse, grayish white thickened multinodular or papular appearance with small red spots in the center.  Red spots are orifices of minor salivary gland duct around which inflammatory cell infiltration is prominent. This may give the appearance of “umblicated swelling”.

NICOTINIC STOMATITIS

HISTOLOGICALLY

 Hyperkeratosis with variable degrees of acanthosis.  Chronic inflammation of palatal mucous glands, their openings are blocked by hyperkeratinization forming red spots.

MANAGEMENT

 The condition is usually reversible if the smoking is stopped (the smoker may use an acrylic palatal plate to protect palate during smoking).

 The condition is generally thought to be benign with little or no risk of malignant transformation.

III. INFECTIVE

A)Candidiasis  Caused by Candida Albicans  It is normally present in oral mucosa.  30%-50% of people carry it  Candida albicans is the most common oral fungal infection in humans.  May be pathogenic in certain situations. ItConsidered to be opportunistic infection.

It may be seen in:  Immunosuppressive cases (AIDS.HIV)  Malignancies( Multiple myloma)  Uncontrolled diabetes mellitus  Xerostomia  Heavy smokers  Corticosteroids therapy  Broad spectrum antibiotics  Extremes of age( neonatal .old age)  Debilitating conditions  Bad oral hygiene especially with complete denture  Pregnant women have infection in vagina

CLINICAL FEATURES:

 Exhibits a variety of clinical patterns

1.Acute Pseudo membranous Candidiasis 2.Acute Erythematous Candidiasis 3.Chronic Atrophic Candidiasis 4.Chronic Hypreplastic Candidiasis 5.Muco-cutaneous Candidiasis

1. PSEUDO MEMBRANOUS CANDIDIASIS(THRUSH)

 It occurs in extremes of age and in new born infant  Characterized by presence of adherent white plaques that resembles curled milk on oral mucosa.  Scraping them with dry gauze reveals a raw erythematous or sometimes normally appearing mucosa.

CAUSES:

 Impairment of immune system (leukemic patients, HIV patients ) leads to chronic slow onset.  Infants with underdeveloped immune system.

SYMPTOMS:

 Mild burning sensation.  Unpleasant taste sensation.  Plaques are distributed on buccal mucosa palate, & dorsal tongue.

PSEUDO MEMBRANOUS CANDIDIASIS

Pseudomembranous candidiasis on the palate. PSEUDO MEMBRANOUS CANDIDIASIS

PSEUDO MEMBRANOUS CANDIDIASIS

2.ERYTHEMATOUS CANDIDIASIS

It occurs due to intake of broad spectrum antibiotics . (Antibiotic Sore Mouth) Clinically : It is presented as a red and often painful area of the oral mucosa(most commonly on the dorsum of tongue) . Histopathologically : The lesion shows thin, atrophic nonkeratinized epithelium with some hyphae and spores in superficial layers. ERYTHEMATOUS CANDIDIASIS (EC) ERYTHEMATOUS CANDIDIASIS

A patient with a history of chronic iron deficiency anemia developed red, raw, and painful areas of the mucosa, diagnosed as acute atrophic candidiasis. 3.CHRONIC ATROPHIC CANDIDIASIS(DENTURE SORE MOUTH)

 This common and usually symptomless condition is found mostly in denture wearers.  Females are more affected than males.  It occurs commonly on the hard patate . Causes: Patients wear the denture rarely cleaning it. improper denture design , allergy to denture base.

Clinically is characterized by :

Different degrees of erythema Petechial hemorrhage localized to the denture bearing areas of maxillary removable dental prosthesis.  It is usually accompanied by angular chelitis which occurs due to:  Loss of vertical dimension  Vitamin B 12deficiency  Folic acid deficiency

 Angular chelitis is characterized by: oErythema oFissuring oScaling  It occurs in older individuals with reduced vertical dimension of occlusion and folds at the corner of mouth. Saliva tend to pool in such areas. progressive stages of denture sore mouth

3.CHRONIC ATROPHIC CANDIDIASIS(DENTURE SORE MOUTH)

 Differential diagnosis includes:  Allergic stomatitis which is allergy to denture acryl.  Median rhomboid glossit is which occurs on dorsum of tongue and might be a developmental anomaly or due to atrophic candidiasis.

4.CHRONIC HYPERPLASTIC CANDIDIASIS (CANDIDAL LEUKOPLAKIA )

 It is presented as a persistent dense white patch of irregular thickness and density with a rough surface.  that cannot be removed by scraping.  Common on anterior buccal mucosa, often bilaterally .  They are associated with angular chelitis .  Either represent:  Candidiasis superimposing on a pre existing Leukoplakic lesion.  or Candidal organism alone capable of inducing a hyperkeratotic lesion .

5.MUCOCUTANEOUS CANDIDIASIS

 Severe oral candidiasis may be seen as a component of relatively rare group of immunological disorders known as mucocutaneous candidiasis.  Severity of candida linfection correlates with the severity of immunological defect.

CHRONIC MUCOCUTANEOUS CANDIDIASIS

TREATMENT

 Local antifungal.  If there is denture sore mouth rebase the denture.  Denture base can be used to place the drug. N.B. In young adults, angular chelitis is a bad sign that it may be suggesting HIV +ve case  Antifungal Agents:  Nystatin(suspension 100KU/mL, or 1% cream)  Amphotercin B  Clotrimazole (troche, 10mg)  Ketoconazole

III. INFECTIVE b) Hairy leukoplakia It is represents an opportunistic infection related to the presence of Epstein –Barr Virus, found almost exclusively in :  HIV patients  organs transplanted patients  pts who are on corticosteroids or chemotherapy Clinical features : It is found mainly along the lateral margins of the tongue . It may be unilateral or bilateral . It presents as a painless well demarcated white lesion that varies from a flat plaque- like lesion to papillary / filiform hair –like projection. Secondary candidal infection of supreficial layer is common . Treatment There is no treatment HAIRY LEUKOPLAKIA