4. INTRODUCTION
White Lesion
lesions of the oral mucosa, which
are white results from:
Thickened layer of keratin
Epithelial hyperplasia
Intracellular epithelial edema
Reduced vascularity of subjacent
connective tissue
7. MECHANICAL (TRAUMATIC)
Frictional (traumatic) keratosis is defined as a
white plaque with a rough surface that is
clearly related to an identifiable source of
mechanical irritation.
Frictional keratosis is frequently associated
with rough or maladjusted dentures and with
sharp cusps and edges of broken teeth.
Treatment: Traumatic keratosis has never
been shown to undergo malignant
transformation.
Upon removal of the offending agent, the
lesion should resolve within 2 weeks. Biopsies
should be performed on lesions that do not
heal to rule out a dysplastic lesion.
8. CHEMICAL (TRAUMATIC)
Transient non-keratotic white lesions of the
oral mucosa are often a result of a variety
of agents that are caustic when retained in
the mouth for long periods of time, such as
Aspirin, Silver Nitrate, Formocresol, Sodium
Hypochlorite, Dental Cavity Varnishes, Acid
Etching Materials, Hydrogen Peroxide.
The lesions are usually located on the
mucobuccal fold area and gingiva.
The injured area is irregular in shape,
white, covered with a pseudo membrane,
and very painful.
9. Treatment and prognosis:
The best treatment of chemical burns of the oral cavity is prevention.
The proper use of a rubber dam during endodontic procedures reduces the
risk of iatrogenic chemical burns.
Most superficial burns heal within 1 or 2 weeks.
A protective emollient agent such as a film of methyl cellulose may
provide relief. Deep-tissue burns and necrosis may require careful
debridement of the surface, followed by antibiotic coverage.
11. LEUKOPLAKIA
Leuko: white Plak: patch
Definition: A predominantly white lesion of the oral mucosa that cannot be
characterized as any other definable lesion.
Leukoplakia is a white keratotic patches that cannot be rubbed off and a
precancerous lesion with a recognizable risk for malignant transformation.
12. AETIOLOGICAL FACTORS OF
LEUKOPLAKIA
Although no particular causative factor has been proven to be related with
leukoplakia but few factors are suggested to be associated with
leukoplakia.
Tobacco ( smoking/Chewable Tobacco).
Alcohol ( no direct relation, although might be associated with smoking).
Candida ( candidal leukoplakia).
Virus( HPV- ROLE UNKNOWN) (EBV –hairy leukoplakia).
13. PRE – MALIGNANT POTENTIAL OF
LEUKOPLAKIA
LEUKOPLAKIA has an unpredictable tendency to undergo MALIGNANT
TRANSFORMATION.
But every lesion WOULD NOT have pre malignant potential.
Combining results of various studies have shown that the rate of malignant
transformation can be as high as 14%.
The wide range of rate of malignant transformation is due to various
reasons such as variation in smoking, betel nut usage, nutritional status
etc.
14. HIGH RISK SITES
Ventral surface of tongue
Floor of the mouth,
Retromolar area
Lingual aspect of alveolar mucosa.
17. NON-HOMOGENOUS LEUKOPLAKIA
Redness (such appearance is known as Speckled Appearance).
Ulceration.
Nodular thickening or heaping up of the surface.
18. INVESTIGATION AND MANAGEMENT
Educate and counseling the patient.
Cessation of the habit.
Removal of the cause (frictional keratoses).
Watchful wait.
If the lesion persist then go for biopsy.
If dysplasia present than excision of the lesion with 1mm normal margins
and sent for histopathology.
Follow up for at least 6 months.
25. MANAGEMENT
Topical corticosteriods (in mild cases restricted to oral lesion) for example
hydrocortisone, betamethasone, cyclosporin and clobetasol.
Topical antifungal.
Systemic corticosteriods (in sever oral and extra oral involvement) for
example prednisolone (1mg/kg/day).
Supportive therapy includes: benzydamine spray/mouthrinses or 2%
lidocaine oral anesthetic gel…avoid spicy citrus food…oral hygiene
maintanance…smoking cessation
26. REFERENCE
Oral Pathology 4th Edition by J V Soames.
Essentials of Oral Pathology and Oral Medicine by R.A. Cawson.
Internet Source.
