white lesions

1. INTRODUCTION TO WHITE AND
RED LESIONS

2.  PREMALIGNANT / PRECANCEROUS LESIONS – It is defined as a
“Morphologically altered tissue in which cancer is more likely to
occur, than its apparently normal counterparts.”
 EXAMPLES –
 LEUKOPLAKIA
 ERYTHROPLAKIA
 CARCINOMA IN SITU
 BOWEN DISEASE
 ACTINIC KERATOSIS, CHELITIS & ELSTOSIS
 MUCOSAL CHANGES ASSOCIATED WITH SMOKING HABITS

3.  PREMALIGNANT / PRECANCEROUS CONDITION – It is defined as a
“Generalized state or condition associated with a significantly
increased risk of cancer development.”
 EXAMPLES –
 ORAL SUBMUCOUS FIBROSIS (OSMF)
 ORAL LICHEN PLANUS (OLP)
 LUPUS ERYTHEMATOSUS (LE)
 SIDEROPENIC DYSPLASIA
 DYSKERATOSIS CONGENITA
 SYPHILIS
 Both the definitions have been put forth by World Health Organization (WHO) in
the year 1978.
 Some authorities prefer the term ‘potentially malignant’ to precancerous /
premalignant because not all precancerous lesions undergo malignant
transformation and a proportion regress or stay the same.

4. CLASSIFICATION
 VARIATIONS IN STRUCTURE &APPEARANCE OFTHE NORMAL
MUCOSA
 Leukoedema
 Fordyces granules
 Linea Alba
 NON KERATOTICWHITE LESIONS
 Habitual cheek biting
 Thermal burns
 Radiation mucositis
 Syphilitic mucous patches
 CANDIDIASIS
 KERATOTICWHITE LESIONSWITH NO INCREASED POTENTIAL FOR
THE DEVELOPMENTOFTHE ORAL CANCER
 Stomatitis Nicotina
 Traumatic Keratoses
 Intraoral Skin Grafts
 Psoriasis
 GeographicTongue

5. CLASSIFICATION
 RED & WHITE LESIONSWITH DEFINEDOR UNCERTAIN
PRECANCEROUS POTENTIAL
 Leukoplakia
 Erythroplakia
 Oral lesions associated with the use of tobacco & alcohol
 Electrogalvanically induced oral white lesions
 Carcinoma in situ
 OSMF
 DLE
 Lichen Planus
 Actinic Keratosis, Chelitis
 Dyskeratosis Congentia
 Oral Lichenoid Reactions

6. White appearance of oral mucosa may be caused by a variety of factors:
 Hyperkeratosis
 Acanthosis
 Intra and extraepithelial accumulation of fluid in the epithelium
 Necrosis of the oral epithelium
 Microbes, particularly fungi can produce whitish pseudomembranes
 increased distance to the vascular bed
 decreased vascularity in the lamina propria
 surface ulceration covered by a keratin cap and collapsed bullae.

7.  White lesions are usually painless, but can be focal, multifocal,
striated or diffuse, and these features may give a guide to diagnosis
:
- Focal lesions : often caused by keratosis
- Multifocal lesions: common in thrush and LP
- Striated lesions: typical of LP
- Diffuse white areas: seen in buccal mucosa in leukoedema, in the
palate in stomatitis nicotinia

8.  Red lesion may develop as a result of atrophic epithelium,
characterized by a reduction in no. of epithelial cells or increased
vascularization
 Red lesions can be :
- focal: the lesion of most concerned is erythroplasia. Telangiectasia can
also cause red lesion
- multifocal: often caused by candidiasis
- Discoid: prominent on tongue in erythema migrans
- Diffuse: mucositis, deficiency states, many infections, but most common –
candidiasis
- Linear: seen on tongue in deficiency states

9. NORMAL VARIANTS

10. Linea alba
 Grayish white line at the level of occlusal
plane
 Lesion is typically bilateral
 Etiology : frictional trauma along the occlusal
plane
 It is not because of rough cusps or insufficient
horizontal overlap of the teeth

11. LINEA ALBA

12. LEUKOEDEMA

common mucosal alteration and it is a variation of the normal mucosa.
90% seen in blacks(Afro-Americans).Variation in the mucosa is visible
more clearly in the darker coloured people.
Frequent site: bilateral buccal mucosa. Rarely in labial, soft palate and
floor of the mouth.
Description: faint, diffuse, filmy appearance with mild wrinkling of the
mucosa.
CANNOT BE SCRAPED. Disappear and fades on stretching of the
mucosa.
Microscopy: thickening of the epithelium, Intracellular oedema in
stratum spinosum.Surface may show thickened parakeratinization.
Rx:
NO Rx and NO malignant change.

13. LEUKOEDEMA

14. FORCES GRANULES
 Fordyce granules appear as rice-like, white or
yellow-white, asymptomatic papules of 1–
3 mm
 Ectopic sebaceous glands
 No treatment is required for Fordyce
granules, except for cosmetic removal of
labial lesions

15. FORDYCE’S GRANULES

16. LEUKOPLAKIA
( LEUKOKERATOSIS )

17. LEUKOPLAKIA { Leuko – White, Plakia – Patch }
 DEFINITION –
“ Leukoplakia is defined as a white patch or plaque that cannot be
characterized clinically or pathologically as any other disease and
which is not associated with any other physical or chemical causative
agent except the use of tobacco” – by WHO.
The term Leukoplakia is strictly a clinical one and does not imply a specific
histopathological diagnosis.

18. ETIOLOGY
Two groups of Leukoplakias have been recognized : Idiopathic
Leukoplakia, in which no etiological factors have been
recognized; and Leukoplakias in which an evident predisposing
factor may be present.
Certain etiologies have been put forth –
1. TOBACCO –
 Tobacco used in any form, either smoked or chewed may
cause production of leukoplakia.
 Leukoplakias that are directly attributable to tobacco habits
are, to a large degree, reversible, and it has been
demonstrated in various studies that cessation of the habit,
causes regression of the lesion.

19. 2. ALCOHOL –
 Alcohol has a strong synergistic effect with tobacco, causes
Leukoplakia.
3. SANGUINARIA –
 People who use toothpaste or mouth rinses containing a herbal
extract Sanguinaria, may develop Leukoplakia. ( Sanguinaria
– associated keratosis )

20. CLINICAL CLASSIFICATION
 ACCORDING TO CLINICAL DESCRIPTION –
 Homogenous – it is completely whitish lesion.
 Flat- it has a smooth surface
 Corrugated – like a beach at ebbing tide.
 Pumice like – with a pattern of fine lines. (cristae)
 Wrinkled – like dry, crackled mud surface.
 Non homogenous –
 Nodular or speckled – characterized by white specks or nodules on
erythematous base.
 Verrucous – slow growing, papillary proliferations above the mucosal
surface that may be heavily keratinized.
 Ulcerated – lesion exhibits red area at the periphery of which white patches
are present.
 Erythroleukoplakia – leukoplakia is present with erythroplakia.

21.  ACCORDING TO ETIOLOGY –
 Tobacco induced
 Non tobacco induced
 Idiopathic
 ACCORDING TO HISTOLOGY –
 Dysplastic
 Non Dysplastic
 ACCORDING TO RISK OF FUTURE DEVELOPMENT OF CANCER –
 High Risk Sites –
 Floor of mouth
 Lateral surface of tongue
 Soft palate
 Low Risk Sites –
 Dorsum of tongue
 Hard palate
 Intermediate group –
 All other sites of oral mucosa

22. STAGING OF LEUKOPLAKIA
 SIZE – It is denoted by L
 L1 – size is less than 2 cm
 L2 – size is in the range of 2-4 cm
 L3 – size is more than 4 cm
 L4 – size is not specified
 CLINICIAL ASPECT – It is denoted by C
 C1 – homogenous
 C2 – non homogenous
 C3 – not specified
 PATHOLOGICAL FEATURES – It is denoted by P
 P0 – no dysplasia
 P1 – distinct dysplasia
 PX – dysplasia not specified in the pathology report

23. OLEP STAGING SYSTEM – BY VAN DER WALL,
2000
 Stage 1 - L1 P0
 Stage 2 - L2 P0
 Stage 3 - L3 P0 or L1 L2 P1
 Stage 4 - L3 P1

24. CLINICAL FEATURES
 Leukoplakia usually affects persons older than 30 years of age.
 It is usually found on buccal mucosa, commissures, lips, tongue and
palate. Less commonly seen on gingiva, alveolar ridge, floor of the
mouth and soft palate.
 Lesions on floor of the mouth, tongue and lip vermillion accounts for
maximum malignant changes
 Leukoplakia appears as an intrinsic white area of the oral mucosa,
sometimes homogenous, sometimes wrinkled, sometimes with a
verrucous or fissured surface.

25.  White patch may vary from being transparent and filmy
in appearance to being dense and thick.
 Surface – surface of the lesion is finely wrinkled or
shrieveled and feel rough on palpation
 Color – it ranges fom white, yellowish, brownish
(tobacco stains), reddish-white
 In some cases, leukoplakia will be a single, discrete and
well circumscribed plaque area, whereas in others there
may be number of lesions distributed.
 Most of the cases will be symptomless. But few patients
might report of feeling of increased thickness of mucosa
or they may complain of burning sensatiion ( in cases of
ulcerated and nodular leukoplakia).

26. CLINICAL TYPES
MILD LEUKOPLAKIA –
 Seldom shows dysplasia
 Usually disappears if habit is discontinued
 They appear as slightly elevated gray or gray-white plaques, which may appear
translucent, fissured or wrinkled
 They can have sharply demarcated borders or they might blend gradually into
normal mucosa

27. HOMOGENOUS LEUKOPLAKIA –
 If the patient continues the habit, mild Leukoplakia slowly extends laterally,
becomes thicker and acquires a distinctly white appearance.
 Affected mucosa at this stage becomes leathery to palpation, and fissures may
deepen.

28. GRANULAR OR NODULAR LEUKOPLAKIA
 Long standing homogenous Leukoplakia can either regress or can become even
more severe with more surface irregularities.
 Small keratotic nodules will be scattered over an atrophic area
 High malignant potential

29. PROLIFERATIVE VERRUCOUS LEUKOPLAKIA
 Characterized by verrucous proliferation above the mucosal surface
 It is slow growing, persistent & irreversible. It begins as simple solitary
hperkeratosis, but tends to become multifocal over period of time. Later it becomes
exophytic and wart like and transforms into a lesion that is clinically and
microscopically identical to verrucous carcinoma.
 Also a high – risk form of leukoplakia

30. SPECKLED LEUKOPLAKIA OR ERYTHROLEUKOPLAKIA
 Some leukoplakic patches demonstrate scattered patches of redness, called as
Erythroplakia. Mixed red-white lesions.
 Such areas represent sites in which epithelial cells are so immature or atrophic that
they can no longer produce keratin
 It reveals advanced dysplasia on biopsy

31. HISTOPATHOLOGICALASPECTS

32. CANDIDIAL LEUKOPLAKIA (Chronic Hyperplastic
Candidiasis )
 In some patients with oral candidiasis, there may be white patch which is non
scrapable. The lesion is bit controversial.
 Some authors believe it is candidiasis which is superimposing on pre-existing
leukoplakic lesion
 Some say candidial organism is capable of producing hyperkeratotic lesion.
 Usually located on anterior buccal mucosa. Usually candidal leukoplakia is of
speckled type.
 Diagnosis is confirmed by presence of candidal hyphae stained with PAS stain.

33. HAIRY LEUKOPLAKIA
 Seen in HIV patients and immunocompromised patients
 It occurs on the lateral margins of the tongue and has a folded, corrugated or ‘hairy’
appearance and generally is asymptomatic
 Candida may be associated with the lesion, but its different from Candidal
leukoplakia
 It is associated with EBV
 Hairy Leukoplakia is a clinical indicator for HIV positive patient turning into full
fledged AIDS patient

34. DIGNOSTIC PROCEDURES
 ELIMINATION OF THE POSSIBLE CAUSES – Clinician should try to rule out
any definable white lesions before accepting a definitive clinical diagnosis of
leukoplakia.
 NON INVASIVE SCREENING TECHNIQUES –
 Cytologic Testing. E.g. Brush Biopsy
 Supravital Dyes. E.g. Toluidine Blue Staining
 DEFINITIVE DIAGNOSTIC TECHNIQUES –
 Biopsy

35. DIFFERENTIAL DIAGNOSIS
 Leukoedema
 Lichen Planus – mostly bilateral and presence of Wickham’s Striae
 Linea Alba – careful history elicits the cause and promotes diagnosis
 White Sponge Nevus – occurs soon after birth.
 Tobacco Pouch Keratosis – careful history & examination
 Electrogalvanic White lesion – disappears when different metal
restorations are replaced with composites
 Frictional Keratosis – chronic mechanical irritation from broken
dentures, root stumps, sharp cusps causes white lesion with keratotic
surface.
 Nicotine stomatitis (Smoker’s palate) – white palatal alteration which
is nothing but hyperkeratotic response to heat generated by smoking

36. TREATMENT MODALITIES
 TOBACCO INDUCED LEUKOPLAKIA (without dysplasia) –
 Cessation of the habit may regress the lesion.
 Clinical evaluation every 6 months.
 NUTRITIONAL THERAPY –
 Isotretinoin (form of vitamin A ) may be helpful
 Vitamin B complex – as a supplement
 Antioxidants – which includes Betacarotene
Supplements, Lycobeta M, Antooxid,Otoxid
 Combination doses of Vitamin A,C & E
 Diet rich in fruits and vegetables

37.  SURGICAL THERAPY – (in cases of marked dysplasia and when lesion doesn’t
subside on removal of etiological factor or from nutritional supplements, and in
cases of idiopathic leukoplakia )
 Surgical excision of the lesion
 Cryosurgery
 LASERS ( Carbon dioxide Lasers )
 Biopsy
 Laser peel
 Ablation
 Fulguration (Electrocauterisation)