WHITE LESION OF ORAL MUCOSA

Dr. Samina

ORAL MUCOSA

DEFINITION
It is defined as a moist lining of oral cavity

that communicates with the exterior.

Mucous membrane are also found lining other

body cavities such as sinuses, GIT, uterus etc.

ORAL MUCOSA
The oral mucosa consists of two layers: an

epithelium (stratified squamous epithelium) & an underlying layer of connective tissue, which is the lamina propria.

Beneath selected areas of the oral mucosa is

a loose connective tissue, the submucosa

ORAL MUCOSA
The Epithelium Keratinization (orthokeratinization) Parakeratinization Nonkeratinization

Orthokeratinized -- no nuclei present Parakeratinized -- pyknotic nuclei retained

keratinisation - organic process by which keratin is deposited in cells

KERATINIZED EPITHELIUM
Most of the oral mucosal surface is lined by

nonkeratinized stratified squamous epithelium except gingiva, hard palate and dorsal surface of the tongue where the epithelium is keratinized

The keratinized cells have no nuclei and the

cytoplasm is displaced by large numbers of keratin filaments Keratinized epithelium is associated with masticatory function and have four layers of cells

MASTICATORY MUCOSA
Basal layer Spinous layer Granular layer Cornified layer

NONKERATINIZED EPITHELIUM
Nonkeratinized epithelial cells in the superfecial

layers do not have keratin filaments in the cytoplasm

The surface cells also have nuclei The stratum corneum and stratum granulosum

layers are absent

This epithelium is associated with lining of the oral

cavity

LAMINA PROPRIA
Is the connective tissue layer immediately below the

epithelium. Can be divided into the papillary layer & reticular layer.
In the papillary layer, finger-like projections of

connective tissue extend into the deep surface of the epithelium. An increase in the number & length of the papillae is seen in areas where mechanical adhesion between the epithelium & lamina propria is required (masticatory mucosa).

Oral Mucous Membrane

Epithelium

Lamina Propria

Submucosa

Periosteum Bone

Oral Mucous Membrane

WHITE LESIONS
Color of oral mucosa:
O.M is translucent & reflect s content of

underlying tissue. Normal color of oral mucosa is PINK but the intensity varies due to factors like;
1 -Thickness of O.M. 2 -Degree of keratinization 3 -Amount of vascularity & fibrous content in C.T. 4 -Formation of pseudomembrain 5 -Pigmentation producing cells like melanocytes

WHITE LESIONS
Color of different location of healthy oral

mucosa:
Masticatory mucosa= light pink
Lining mucosa

=reddish pink Palatoglossal arch =dusky red (due to increase vasculrity.)

WHITE LESION
.It is a non specific term used to describe any abnormal area of o.m that on clinical examination appears whiter than surrounding tissue. It is usually slightly raised ,roughened or of different texture than adjacent normal mucosa.

WHITE LESIONS
REASON OF WHITE APPEARANCE:
Increase thickness of epithelium with increase

production of keratin (hyperkeratosis) & production of abnormal keratin & imbibitions of fluid by upper layer of mucosa Pseudomembrain; occur in coagulation of tissue surface e.g. burn

RED LESION
Refers to an area of reddened mucosa that

may appear red and atrophic or exhibits granular, velvety texture. These lesions may occur alone or in combination with white lesions. Such lesion may termed as a MIXED or RED & WHITE lesions

RED LESIONS
Reasons for appearance of red lesions:
Dilated blood vessels Influx of new blood vessels Hemorrhage under epithelium Relatively thin outer epithelium

RED & WHITE LESIONS etiologic classification

1) NORMAL MUCOSAL VARIATION -Leukoedema - Fordyce granules ( sebaceous gland) - linea alba buccalis 2) GENITICALLY LINKED WHITE KERATOTIC LESION -oral genodermatoses -white sponge nevus -Hereditary benign intraepithelial dyskeratosis -Pachyonychia congenita (pachy=thick onyx=nail _abnormal thickening of Nail) 3) Post inflammatory white lesions -Traumatic keratosis -Mechanical trauma -thermal burn - chemical burn -radiation mucositis -reactive mucosal hyperplasia (stomatitis nicotina palati)

RED & WHITE

etiologic classification
-syphilis 4) WHITE & RED LESIONS DUE TO INFECTIONS

-Measles (koplik,s spot)

-candidiasis -Bacterial stomatitis 5) PREMALIGNANT LESIONS

-Leukoplakia
-Lichen planus -Lichenoid reaction -Erythroplakia

-Acitinic keratoses
-Discoid lupus erythmatosus -Chronic hyperplasic candidiasis

6) PREMALIGNANT CONDITIONS -Oral submucous fibrosis -Oral psoriasiform -Dyskeratosis congenita -Sydropenic dysphagia -Syphilitic glossitis 7) MISCELLANEOUS

White lesion of oral cavity

Non- scrapable ( keratotic) Linea alba buccallis
Frictional/traumatic keratosis Homogenous leukoplakia Reticular lichen planus Chronic hyperplasic candidiasis Dyskeratosis congenita White sponge nevus

Scrapable (non-keratotic ) Chemical/thermal burn

Pseudo membranous dandidiasis Syphilitic mucous patch Diphtheric patch

FORDYCE GRANULE
ectopic collections of sebaceous glands

upper lip, buccal mucosa, gingiva, anterior pillars of fauces bilaterally symmetrical distribution 60-70% of adult population granules in upper lip increases during puberty; granules in buccal mucosa increases in later stages of life multiple, small, discrete, milia-like, yellowish stuctures; 1-2mm diameter occasionally form slightly raised confluent plaques

FORDYCES NODULE

LEKODEMA
more in blacks than whites possibly due to

mucosal pigmentation in blacks making edematous changes more noticeable variation of normal rather than disease more common and severe in smokers (?) diffused, gray-white, milky, opalescent mucosa folded surface, wrinkles or whitish streaks lesions do not rub off bilateral, may extend onto labial mucosa easy to diagnose: white appearance diminishes when cheek is stretched

LEUKODEMA
Increased thickness of epithelium with striking intracellular edema of spinuos layer Vacuolated cells appear large and have stretched nuclei Parakeratinized epithelial surface Broad and elongated rete ridges Benign condition

Pachyonychia congenita
Autosomal dominant hereditary condition Gross thickening of nails Palmoplanter kertosis Oral lesion white opaque patches on

dorsum & lateral borders of tongue & cheeks

Dyskeratosis congenita
Hereditary disorder with Male predilection Abnormal pigmentation of skin, dystrophic

nails & hyperkeratosis of mucous membrane Severe gingivitis & periodontal destruction

Follicular keratosis (Darier`s disease)

Autosomal dominant disorder Mutation in genes that encode an intrcellular

calcium pump abnormal desmosomal organization Multiple heavily keratinized papules on forehead, scalp & ears, become secondarily infected & foul smelling Oral lesions whitish coalescing papules on hard palate & gingiva

Darier`s disease

Histological features; hyperkeratosis, suprabasal cleft containing acantholytic cells Large abnormally keratinized squamous cells (Corps ronds) & smaller flattened cells (grains) seen in the roof of cleft

DARIER`S DISEASE

FRICTIONAL /TRAUMATIC KERATOSIS

Defined as a white patch with a rough surface which is clearly related to a source of mechanical

irritation & that will disappear over a time with removal of stimuli. -a) linea alba buccalis:nonscrapable line present on buccal mucosa usually along plane of occlusion.
b) chronic lip,cheek,tongue chewing c) Due to rough flanges of denture Management: -removal of etiologic agent -symptomatic treatment

CHEMICAL BURNS & THERMAL BURNS

Chemical burns

Analgesics like aspirin, clove oil etc, Phenol ,silver nitrate ,conc. H2O2 ,RCT medicaments. Intake of hot food & beverages

Thermal burns

D.Dx.
Acute pseudomembranous candidiasis Gangrenous stomatitis

Treatment:
1) topical application of anasthetic agent like benzocain/lignocain Gel( choline salicylate 8.7%,benzylkonium0.01% & lignocain Hcl 2%) 2) Topical application of steroids e.g. Triamcinolone acetonide oral past 1%. 3) Analgesics for sever pain.

NICOTINE STOMATITIS,STOMATITIS NICOTINA PALATINUS,SMOKERS PALATE

This lesion is a reactive hyperplasia to the heat

generated by the tobacco smoke that act as a chronic irritating agent. Mostly seen in reverse/ chutta & pipe smokers & less in beedi. Cigarette smokers.

NICOTINIC STOMATITIS
C/F.
Usually seen in males Generally asymptomatic e.g. No pain Palatal mucosa appear as a diffuse grayish white

surface or flat top nodules with red pin point areas situated in center of nodules. Red pin point areas correspond to the inflamed orifices of minor salivary glands ducts.

D.DX.
Palatal papillary hyperplasia Focal epithelial hyperplasia (Hecks disease) Darier,s disease ( follicular keratosis )

Histopathological features
Hyperkeratosis & Acanthosis of palatal

epithelium Mild patchy chronic inflammation of sub epithelial connective tissues & mucous glands Squamous metaplasia of excretory ducts Treatment The palate will return to normal usually within 1 to 2 weeks of smoking cessation High risk areas should be examined closely

WHITE SPONG NEVUS

It is a hereditary dyskeratotic hyperplasia of the mucous membrane that shows an autosomal dominant inheritance pattern with irregular penetrance. Mutation in genes coding for keratins 4 & 13

It is also known as white folded gingivostomatitis,

Familial white folded hypertrophy of the mucous membrane leukokeratosis oris, hereditary leukokerarosis , leukoderma exfoliativum mucosa oris & nevus spongiosus albus mucosae.

Aetiopathogenesis:
Basic defect lies in epithelial cell maturation & desquamation. There is decreased shedding of keratin which leads to white sponge

nevus C/F:
Usually present at birth or early childhood There in no sex predilection. Involve O.M but other mucosal sites also e.g. nasal cavity , esophagus ,

larynx.
Present as an asymptomatic gray white folded or corrugated spongy

mucosal lesion
Mucosal lesions have a soft or spongy texture & white opalescent hue. Few millimeters to several centimeters It is usually asymptomatic, but can become symptomatic if secondary

infection occur

WHITE SPONGE NEVUS

D.DX. -leukoedema ,leukoplakia ,traumatic keratosis, chemical burn,candidiasis, lichen planus, pachyonychia congenita , Dariers disease & dyskeratosis congenita. HISTOPATHOLOGICAL FEATURES:

Epithelial thickening showing both acanthosis &

hyperkeratosis. Mild inflammatory cell infiltrate is seen in sub mucosa.

TREATMENT: -If asymptomatic =no treatment -If symptomatic = tetracycline M/W & penicillin.

ORAL LICHEN PLANUS (OLP)

Derived from Greek literature
Lichen=tree moss & planus=flat

Definition:
Olp is a common chronic immunological

inflammatory mucocutanious disorder that varies in appearance from keratotic to erythematous & ulcerative

 ETIOPATHOGENESIS:
Exact etiology is unknown Olp is T cell mediated disorder in which there is

production of cytokines which leads to apoptosis.

C/F:

Commonly affect 1-2% of population 25% occur on oral mucosa alone 35% occur on cutaneous surface alone 40% occur on both oral & cutaneous surfaces Female: male 2:1

ORAL LICHEN PLANUS

C/F:
Characteristic appearance of white papules that

usually coalesce forming a network of lines that may intersect or crisscross each other forming various patterns. SKIN INVOLVMENT:
Lesion is itchy & violaceous to brown papules frequently over flexor aspect of wrist or ankle . ALOPECIA-loss of hair when scalp is involved. ONYCHORRHEXIS longitudinal ridging & grooves ANONYCHIA permanent nail loss

ORAL LICHEN PLANUS

C/F:
ORAL MANIFESTATION: Basic lesion is papule arranged in linear or annular forms &

criss crossing each other forming various pattern like annular & reticular forms. Six types Reticular (a net work) , papular , plaque like (a small circumscribed area distinct from surrounding surface in character & appearance) , erosive atrophic & bullous .

D.DX: 1) Lichenoid drug reaction 2) Hyperplasic candidiasis 3) Electrogalvanic white lesions 4) Lupus erythmatosis 5) Frictional keratosis 6) Graft versus host reaction 7) Leukoplakia

histopathology
Orthokeratosis / parakeratosis

Reteriges may be absent or hypertroplastic

Pointed saw tooth shaped Destruction of basal cell layer

Intense band like infiltrate of T-lymphocytes immediately subjacent to epithelium

ORAL LICHEN PLANUS

INVESTIGATIONS:
Dx. Achieved by clinical presentation Biopsy may be complementary .

COMPLICATION:
It can developed into carcinoma(SCC) specially

erosive form.

MANAGEMENT:

If asymptomatic then requires no specific treatment except

chlorhxidine M/W to stop secondary infection & follow up once three months.

If atrophic & ulcerative Topical steroids (triamcinolone acetonoid 0.1%) Triamcinolone oral suspension 40-80 mg /day prednisolone 5-7 days reducing to 510mg over 2-4-weeks Injection into site of prednisolone 10-20mg/ml every 2-4 weeks Antifungal to stop candidiasis -- Antihistamins --cyclosporines, Azathioprine Surgery:
Excision, laser , cryosurgery,

ORAL SUBMUCOUS FIBROSIS

OSF is a chronic, progressive, scarring, high

risk precancerous condition of oral mucosa seen primarily in Indian subcontinent, South east Asia, Taiwan& China.

ORAL SUBMUCOUS FIBROSIS

It is a chronic disease affecting any part of oral cavity. Role of Areca nuts (arecoline & tannin) in disturbing homeostatic

equilibrium between synthesis & degradation of extracellular matrix activated inflammatory cells cytokines , growth factors fibrosis collagen synthesis down regulating collagenase Copper in areca increases activity of enzym Lysyl oxidase

Occasionally it is preceded & associated with vesicle formation & then

followed by the hylinization of the lamina propria. Later subepithelial & submucosal myofibrosis leads to stiffness of O.M.

 ETIOPATHOGENESIS:
Still unclear but it is believe to be multifactorial ; Chewing of betel nut is one of the most etiologic

factor Nutritional deficiency : anemia ,iron vitamins , proteins Genetic factors

C/F:
Common age is 12-40 years Burning sensation , blanching of O.M. May involve buccal mucosa, retromolar area ,soft

palate,uvula & tongu

ORAL SUBMUCOUS FIBROSIS

C/F:

Small & stiff tongue Blanched & leathery floor of the mouth Fibrotic & depigmented gingiva Rubbery soft palate & blenched atrophic tonsils Trismus ,impaired mouth movements (whistling, eating blowing. Hearing loss due to stenosis of Eustachian tubes Dryness of mouth Dysphagia to solids

INVESTIGATIONS:Dx. Clinical finding Incisional biopsy Raised ESR D.DX.:

Scleroderma , anemia amyloidosis

Histopathology
Submucosal deposition of dense & hypo

vascular collagenous connective tissue Variable number of inflammatory cells Epithelial changes: Sub epithelial vesicles in early lesion Hyperkeratosis & marked epithelial atrophy in older lesions Epithelial dysplasia in 10-15 % of cases Carcinoma in 6 % of cases

CONNECTIVE TISSUE-NORMAL MUCOSA

GRADE- III , OSMF

OSMF
TREATMENT 1) HABIT CONTROL 2) EXERCISE OR PHYSIOTHERAPY 3) MEDICINES

Cortico steroids ( Dexamethasone & Betamethasone) Antioxident (Beta-Carotene, Zn sulfate, Curcumine, Mg, Cu) Proteolytic enzymes ( Hyluronidase & placenta-extracts) Anticytokines (VB6, integrine) Newer drugs: Pentoxifylline ,interferon -( anti-fibrotic cytokine), levamosol, lycopene

4)

SURGICAL Surgical relieving of fibrous bands with buccal pad of fats covering the wound.

O.S.M.F
TREATMENT:

1) HABIT CONTROL 2) EXERCISE OR PHYSIOTHERAPY:

Microwave Diathermy +Stretching exercises

3) MEDICINES:
SYSTEMIC:

Iron supplements & vitamins. Antioxident capsule bid for 3 months ( Beta Carotene, Zn sulfate, CURCUMIN, Mg, Cu) Immunomodulators: Levamisole 150mg OD for 3 days twice in a month for 3 month

TOPICAL: (corticosteroids)

Benzydamine 0.15% M/W Triamcenolone Gel or crushed Dexamethasone tablet in 20 ml water as M/W.

INTRLESIONAL INJECTIONS:

DEXAMETHASONE + HYLURONIDASE + LIGNOCANE multiple site once a week for 6 weeks BETAMETHASONE +HYLURONIDASE +LIGNOCANE +PLACENTA EXTRACTS =3ML Interferon gamma injection

4) SURGICAL:

in sever trismus or dysplastic changes but excision can result in contracture of tissue.

PROGNOSIS:

Is not good..
COMPLICATION: Can transformed into S.C.C. (7-14%) according to Cawson 25%

ORAL LEUKOPLAKIA
It is the most common precancerous lesion . DEFINITION:
It is often confusing & controversial. WHO definition :(1978) Leukoplakia is a white patch or

plaque that can not be characterized clinically or pathologically as any other disease.

ETIOPATHOGENESIS:

1) tobacco (smoke & smokeless form) 2) alcohol 3) viral infection possibly Human Papilloma Virus 4) diabetes mellitus 5) candidiasis may be primary cause or superinfaction 7) dietary factors vitamin A,B12 ,C ,E

ORAL LEUKOPLAKIA
TYPES OF LEUKOPLAKIA

1) Homogeneous -2) Non-homogeneous Homogeneous L. appears white uniform , flat lesion that may exhibit shallow cracks & has smooth , wrinkle or corrugated surface with consistent texture. Non-homogeneous L. appears white or white & red (erythroleukoplakia) lesion that may be either irregularly flat , nodular or exophytic.

FEATURES ASSOCIATED WITH INCREASE MALIGNAT TRANSFORMATION:

Gender ; women seems to be at increase risk Long duration of leukoplakia Leukoplakia in non-smokers Location in floor of mouth & tongue Non-homogeneous type Presence of Candida albican Presence of epithelial dysplasia

ORAL LEUKOPLAKIA
DDX: from carcinoma, lichen planus, thrush INVESTIGATIONS:
TOLUDINE BLUE STAINING; clinically stains

malignant lesions , but not normal mucosa.

It also serves as a guide to biopsy

CYTOBRUSH TECHNIQUE ; BIOPSY Incisional & excisional

D.DX.
Chronic hyperplastic candidiasis Reticular lichen planus White sponge nevus

ORAL LEUKOPLAKIA
TREATMENT:
1. General consideration- all possible white keratotic agent should be eliminated (sp. smoking) 2.Topical antifungal- Clotrimazole cream thrice/day for a week. If reduction in size continue 1 month. 3. NO RESPONSE: If less than 1 cm -Exicisional biopsy If more than 1 cm- Incisional boipsy
dysplasia absent - RETINOL-A ointment bid/1 month. dysplasia present
;total excision of lesion with graft ( follow up once in 6 months for 3 years) If excision not possible A) Cap.Lycopene .4mg -8mg for 3 months B) Cap.Antioxidants with selenium bid 6 months C) topical Bleomycin 1% thrice /day for 15 days

LUPUS ERYTHEMATOSIS
Collagen vascular /Connective tissue disease Autoimmune process Mostly females affected 3 clinicopathological forms 1) SLE, 2) CCLE, 3) SCLE Systemic LE (SLE) multisystem disease Cutaneous + oral manifestations increase activity of B-lymphocytes abnormal funtion of T-lymphocytes

SLE
Clinical features kidneys, cardiac involment Oral lesions: 40% Palate, buccal mucosa & gingivae Lichenoid areas/ granulomatous lesions Lupus cheilitis ( vermilion zone of lower lip) Ulceration, pain erythema & hyperkeratosis

Chronic Cutaneous LE
Skin lesions
Discoid Lescaly erythematous distributed on sun-

exposed skin of head & neck Cutaneous atrophy & scarring hypo/ hyper pigmentation

ORAL LESIONS Like Erosive lichen planus Ulcerated / atrophic central zone surrounded by white fine , radiating striae Painful when exposed to acidic/ salty foods

Histopathological features

Hyperkeratosis Alternating atrophy & thickning of spinous layer Degeneration of basal cell layer Subepithelial lymphocytic infilteration D/D Distinguished from LP by patchy deposits of PAS-positive material in basement membrane, subepithelial edema & perivascular inflammatory infiltrate Direct Immunofluorescence study

Treatment
Avoid sun exposure

NSAIDs + antimalarials
Topical; steroids

Prognosis 5 yrs survival rate is 82%- 90% Most common cause of death is renal failure

THANKS FOR LISTENING