Dr.RajeshDr.Rajesh

GOOD AFTERNOONGOOD AFTERNOON

LESIONS

Macules•Well-circumscribed, flat lesions that are

noticeable because of their change from normal

skin color.

•They may be red due to the presence of vascular

lesions or inflammation, or pigmented due to the

Presence of melanin, hemosiderin, and drugs.

Solid lesions raised above the skin

surface that are smaller than 1 cm

in diameter. Papules may be seen

in a wide variety of diseases

including erythema multiforme

simplex, rubella, lupus

erythematosus, and sarcoidosis.

Papule

Solid raised lesions that are

over 1 cm in diameter; they are

large papules.

Plaques

These lesions are present deep in

the dermis,and the epidermis can

be easily moved over them.

Nodules

Elevated blisters containing clear fluid that are under 1 cm in diameter.

Vesicles

Elevated blister like

lesions containing

clear fluid that are over

1 cm in diameter.

Bullae

Moist red lesions often caused by

the rupture of vesicles or bullae as

well as trauma.

Erosions

WHITE WHITE LESIONSLESIONS

A Non specific term used to describe any

abnormal area of the oral mucosa that on

clinical examination appears whiter than the

surrounding tissue and is usually slightly raised

,roughened or of a different texture from

adjacent normal tissue.

Red LesionRed Lesion

Any area of reddened mucosa that may be

smooth and atrophic looking or exhibits a

granular, velvety texture

Precancerous Lesions: defined as a morphologically altered tissue in which cancer is more likely to occur. e.g.Leukoplakia , Erythroplakia, Actinic chelitis, PalatalChanges with Reverse smoking.

Precancerous condition: defined as a generalised state associated With significantly increased risk of cancer. e.g. Syphilis, OSMF, Siderophenic dysphagia, Erosive Lichen Planus, DLE.

PREMALIGNANT CONDITION IN DETAILSPREMALIGNANT CONDITION IN DETAILS

ORAL SUBMUCOUS FIBROSISORAL SUBMUCOUS FIBROSIS

ACTINIC KERATOSISACTINIC KERATOSIS

DYSKERATOSIS CONGENITADYSKERATOSIS CONGENITA

XERODERMA PIGMENTOSUMXERODERMA PIGMENTOSUM

PEUTZ JEGHERS SYNDROME PEUTZ JEGHERS SYNDROME

TERTIARY SYPHILISTERTIARY SYPHILIS

BOWEN’S DISEASE BOWEN’S DISEASE

EROSIVE LICHEN PLANUSEROSIVE LICHEN PLANUS

DISCOID LUPUS ERYTHEMATOUSDISCOID LUPUS ERYTHEMATOUS

PLUMMER VINSON SYNDROMEPLUMMER VINSON SYNDROME

White lesions classificationWhite lesions classification HEREDITARY WHITE LESIONSHEREDITARY WHITE LESIONS REACTIVE INFLAMATORY WHITE LESIONSREACTIVE INFLAMATORY WHITE LESIONS INFECTIOUS WHITE LESIONS INFECTIOUS WHITE LESIONS IDIOPATHIC TRUE LEUKOPLAKIAIDIOPATHIC TRUE LEUKOPLAKIA BOWENS DISEASEBOWENS DISEASE ORAL LICHEN PLANUSORAL LICHEN PLANUS LICHENOID REACTIONSLICHENOID REACTIONS DEVELOPMENTAL- ECTOPIC LYMPHOID TISSUEDEVELOPMENTAL- ECTOPIC LYMPHOID TISSUE FORDYCES GRANULESFORDYCES GRANULES GINGIVAL CYSTS OF ADULT N NEW BORNGINGIVAL CYSTS OF ADULT N NEW BORN MISCELLIANEOUSMISCELLIANEOUS

HEREDITARY WHITE HEREDITARY WHITE LESIONSLESIONS

LEUKODEMALEUKODEMA WHITE SPONGY NEVUSWHITE SPONGY NEVUS HEREDITARY BENIGN HEREDITARY BENIGN

INTRAEPITHELIAL DYSKERATOSISINTRAEPITHELIAL DYSKERATOSIS DYSKERATOSIS CONGENITADYSKERATOSIS CONGENITA

REACTIVE INFLAMMATORY REACTIVE INFLAMMATORY WHITE LESIONSWHITE LESIONS

LINEA ALBA.LINEA ALBA. FRICTIONAL KERATOSIS.FRICTIONAL KERATOSIS. CHEEK CHEWING.CHEEK CHEWING. CHEMICAL INJURIES OF ORAL MUCOSA.CHEMICAL INJURIES OF ORAL MUCOSA. ACTINIC KERATOSIS.ACTINIC KERATOSIS. SMOKELESS TOBACCO INDUCED KERATOSIS.SMOKELESS TOBACCO INDUCED KERATOSIS. NICOTINE STOMATITIS.NICOTINE STOMATITIS. SANGUINARIA INDUCED LEUKOPLAKIASANGUINARIA INDUCED LEUKOPLAKIA

DEVELOPMENTAL WHITE LESIONS DEVELOPMENTAL WHITE LESIONS ——ECTOPIC LYMPHOID TISSUEECTOPIC LYMPHOID TISSUE

FORDYCES GRANULESFORDYCES GRANULES

GINGIVAL CYSTS OF NEW BORN N GINGIVAL CYSTS OF NEW BORN N ADULTS.ADULTS.

MISSELLANEOUS LESIONSMISSELLANEOUS LESIONS GEOGRAPHIC TONGUEGEOGRAPHIC TONGUE HAIRY TONGUEHAIRY TONGUE

LicheLichen n

PlanPlanusus

Definition

FITZ PATRICK et al-1993 defined Lichen

Planus as a unique cutaneous entity

consisting of an eruption of papules distinct

in color and configuration, in patterns and

location of appearance and in microscopic as

well as gross structure.

TYPES

ReticularReticular AnnularAnnular Plaque(hypertPlaque(hypert

rophic)rophic) PapularPapular

ErosiveErosive BullousBullous AtropicAtropic PigmentedPigmented

ETIOLOGY

Interplay of host,lifestyle and environmental

factors

Cell-mediated immunity initiated by

endogenous or exogenous factors.

EXOGENOUS/ENDOGENOUS FACTORS

GeneticGenetic Dental materialsDental materials DrugsDrugs Infectious agentsInfectious agents Auto immunityAuto immunity ImmunodeficiencyImmunodeficiency

Food allergyFood allergy StressStress HabitsHabits TraumaTrauma DM & HTNDM & HTN MalignanciesMalignancies IBDIBD

PATHOGENESIS

Unknown Antigen enters OMM

Antigen presentation by langerhans cells of OMM

T.cell activation

Increase in local cytokine production

Intense inflammatory reaction

Basal cell degeneration

Basal cell degeneration

Pyknotic and shrunken basal cells(civatte bodies)

Apoptotic cell

Phagocyotosed

Incapable of phagocytosis

Extruded into the underlying dermis(colloid bodies)

CLINICAL FEATURES

•Disease of middle aged,females and elderly

•Except for erosive and Bullous forms all other

forms are frequently painless and unrecognized by

the patient.

•About 50 % of patients have skin lesions

•Skin lesions are flat-topped papules with

violaceous hue and a fine scaly surface.

RETICULAR FORM

•Consists of slightly elevated,fine,whitish lines(wick

ham's striae)that produce either a lace like lesion or

a pattern of fine radiating lines(linear) or annular

lesions.

•Lesions are bi-lateral

•Cheeks and tongue are commonly affected

•Papular,plaque,atrophic and erosive lesions are

frequently associated with reticular form.

PAPULAR AND PLAQUE TYPE

•0.5-1 mm whitish elevated areas or papules

are usually seen,plaque like lesions are also

seen that cannot be differentiated from

leukoplakia.

•Seen on keratinized and non-keratinized

mucosa

ATROPHIC

•Appears as erythmatous areas

surrounded by reticular elements.

•Affects the gingiva also and gives a

bright red edematous pattern

involving the full width of attached

gingiva(desquamative gingivitis)

EROSIVE

• Probably develop as a complication of atrophic

process and not necessarily Bullous lesions.

•Occurs more on the buccal mucosa

•A pseudo membrane covers the lesion

BULLOUS

•Rarely observed form

•Bullae and vesicles range from few mm-

several cm.,short-lived and rupture into

ulcers.

•Seen in postero-inferior aspect of the buccal

mucosa

•Striae to be seen here also.

DIFFERENTIAL DIAGNOSIS

Reticular-lichenoid reactions

Plaque-leukoplakia,hyper plastic

candidiasis,traumatic keratosis.

Atrophic-speckled leukoplakia,anemic

stomatitis,SLE and DLE.

Erosive and Bullous-vesiculo-bullous lesions.

Annular-erythema circinata migrans

INVESTIGATIONS

HB%,CT & BTHB%,CT & BT

BiopsyBiopsy

ImmunofluoroscenceImmunofluoroscence

IMMUNOFLUOROSCENCE

•Positive direct

Immunofluoroscence, at the level of

BM

•Pattern may be globular or linear.

TREATMENT

Reasons to treat:

Symptomatic cases

Malignant potential(erosive LP)

TREATMENT

AsymptomaticSymptomatic

Reassurance Treat

SYMPTOMATIC CASES

Candida No Candida

Mild symptomsMild symptoms

Severe symptoms Severe symptoms

Topical steroidTopical steroid

Systemic steroidSystemic steroid

+Topical anti fungal Topical anti fungal+

Symptomatic maintenance with topical anti-fungal and topical steroids

Ulcers resistant to heal

Add intralesional steroids

Symptomatic maintenance therapy

TOPICAL STEROIDS

•Triamcinalone acetate 0.01%

•Clobetasol propionate

•Flucinonide

SYSTEMIC STEROIDS

PREDNISOLONE 20-40 mg

early morning once a day

(taper gradually)

OTHER MODALITIES

Topical cyclosporine rinses

Systemic azathioprine

Levamisole(immuno modulator)

Dapsone (immuno modulator)

Surgery (lasers, cryo)

Photo-chemo therapy(PUVA)

Magneto therapy

Reflexo therapy

EROSIVE LICHEN PLANUS

Malignant potential-2.7%

Treat with topical/systemic

vitamin A for reversal of

dysplastic changes.

OSMFOSMF

DEFINITION

An insidious chronic disease affecting any part of the oral cavity & sometimes the pharynx occasionally preceded by &/or assoc with vesicle formation and always assoc with juxtaepithelial inflammatory reaction,followed by a fibro elastic change of laminapropria with epithelial atrophy leading to stiffness of oral mucosa and causing trismus and inability to eat

ETIOLOGY

ARECANUT CHEWING WITH GENETIC PREDISPOSITION

PATHOGENESISArecanut

Arecoline(5-7%) Alkaloids(0.15-0.6%)Tannins(11-26%)

Fibroblast proliferation

Stimulates collagen synthesis

Collagen fibrils resistant to human collagenase

PATHOGENESISARECANUT ARECANUT CHEWING

OSMFMUSCLE CONTRACTION

JUXTA EPITHELIAL HYALINIZATION

VASO OBLITERATION

DIMINISHED BLOOD SUPPLY

OVER ACTIVITY

GLYCOGEN DEPLETION

MUSCLE FATIGUE AND DEGENERATION

FIBROSIS AND SCARRING OF THE MUSCLE

CLINICAL FEATURES

•Any age - 20 – 60 yrs predominantly

•Male predominance

Symptoms:

•Burning sensation of the oral cavity aggravated by

spicy/hot food/fluids

•Vesiculation, excessive salivation,

ulceration, pigmentation,

recurrent stomatitis, defective

gustatory sensations and dryness

of mouth.

•Gradual stiffening of oral mucosa

after few yrs.

•Difficulty in swallowing when

fibrosis extends to pharynx and

esophagus

•Referred pain in ears, deafness and

nasal voice

•Blanching ,which imparts Marble-like

appearance to the oral mucosa.May be

localized,diffused or lace -like network.

•As disease progresses mucosa becomes stiff and

vertical fibrous bands appear.

SIGNS

In lip-circular bands appear. (Circum

rima oris)

In severe involvement of the lip-lips

become leathery, difficult to avert

In palate-bands radiate from the

pterygomandibular raphe to the

anterior faucial pillars.

Faucial pillars - thin and short.

•Tonsils- may be pressed between the faucial

pillars.

•Soft palate -Mobility is restricted when is

involved.

•Uvula-shrunken bud like or hockey stick

appearance

•Tongue-devoid of papillae, stiff

with impaired protrusion in

severe cases

•Floor of the mouth-blanched

and leathery

•Petechiae seen in 1/5th of

cases.

CLINICAL AND FUNCTIONAL STAGING

Haider et al 2000 BJOMS

Clinical staging

•Stage 1-faucial bands only

•Stage 2-faucial and buccal bands

•Stage 3-faucial,buccal and labial bands

Functional staging

•A –mouth opening >20mm

•B-mouth opening 11-19 mm

•C-mouth opening < 10 mm

INVESTIGATIONS

•Increased ESR

•Anemia

•Eosinophilia

•Increased IgG

•Decreased serum iron

•Increased total Fe binding capacity

•Decreased total saturation of transferrin

•Decreased total serum iron

Treatment

Elimination of the habit

Nutritional support

Bland diet

Cases without bands-topical corticosteroids

Cases with bands-intra-lesional corticosteroids

Physiotherapy

Retinoids

TREATMENT MODALITIES

Intra lesional - cortico steroids

Intra lesional - cortico steroids with hyalurinadase

Systemic – Levamisole/Dapsone

Soft lasers

Turmeric oil

Homeopathy(calcaria florica)

Formulations and dosage

Dexamethasone – 2ml (1ml on each side surrounding the bands)-biweekly for 10 weeks

Hydrocortisone – 1.25 ml once a week for 12 weeks

Dexamethasone – 2ml+hyalurinadase 1500 IU,biweekly for 10 weeks

Hydrocortisone – 1ml+ hyalurinadase 1500 IU,biweekly for 10 weeks

ACITINIC(SOLAR)

KERATOSIS/

ELASTOSIS /CHELITIS

DEFINITION

IS A PREMALIGNANT SQUAMOUS

CELL LESION DUE TO LONG TERM

EXPOSURE TO SOLAR RADIATION.

CLINICAL FEATURES

•Seen on skin,Vermillion border of the lip as a

crusted and Keratotic lesion.

•Labial mucosa exposed to the sun- white area of

atrophic epithelium develops underlying scarring of

lamina propria( referred to as Elastosis )

•Malignant transformation (10%)

TREATMENT

Topical 5-fluoro uracil

Surgical lip shaving procedures

Topical steroids in between treatments to control lip swelling

LEUKOEDEMA

Occurs in 15-35 yrs old.

M:F =2:1

Highest in Blacks(USA),lowest in Indians

The buccal mucosa exhibiting a grayish-

white ,slightly folded ,opalescent appearance with

normal softness and flexibility is termed leukodema.

This change temporarily eliminated by stretching the

mucosa,but re-establishes itself immediately.

Melanin pigmentation enhances opalescence

LINEA LINEA ALBA ALBA

BUCCALISBUCCALIS

The line of keratinization usually found

on the non-keratinized buccal mucosa

parallel to the line of occlusion and

expanding to a triangular area in the

retro-commisure.

FORDYCE’S FORDYCE’S GRANULESGRANULES

FORDYCE’S GRANULESFORDYCE’S GRANULES

Ectopic presence of tubulo-acinar sebaceous glands in

oral cavity.

Appears in 80-90 % of adult population.

Appears as small ,white/yellowish sub-mucosal

plaques.

Seen on Vermillion border, buccal

mucosa, occasionally on the palate ,

gingiva and the tongue.

No specific function/does not

increase with age.

Occasionally transforms into

pseudo cyst/sebaceous adenoma.

WHITE SPONGY NEVUSWHITE SPONGY NEVUS

EtiopathogenesisEtiopathogenesis : Mutations in : Mutations in Genes Genes

Coding For Epihtelial Keratin Of Type K4 N K33.Coding For Epihtelial Keratin Of Type K4 N K33.

::Clinical features:Clinical features:

Age:18 –22yrs….Age:18 –22yrs….

M=f.Autosomal Dominant Disorder….M=f.Autosomal Dominant Disorder….

Site : Buccal Mucosa.Site : Buccal Mucosa.

Extra Oral Sites : Oesophagus,anogenital Mucosa.Extra Oral Sites : Oesophagus,anogenital Mucosa.

..Management: Management: No Specific Treatment RequiredNo Specific Treatment Required..

WHITE SPONGY NEVUSWHITE SPONGY NEVUS

NICOTINE STOMATITISNICOTINE STOMATITIS

ETIOLOGYETIOLOGY: HEAVY CIGARETTE ,PIPE ,CIGAR SMOKING.: HEAVY CIGARETTE ,PIPE ,CIGAR SMOKING.

C/F:NUMEROUS ELEVATED PAPULES WITH RED PUNCTATED C/F:NUMEROUS ELEVATED PAPULES WITH RED PUNCTATED

CENTER…… INFLAMMED SALIVARY GLAND WITH ALTERED CENTER…… INFLAMMED SALIVARY GLAND WITH ALTERED

DUCTS.DUCTS.

HISTOPATHHISTOPATH:HYPERKERATOSIS,SQUAMOUS :HYPERKERATOSIS,SQUAMOUS

METAPLASIA,MILD TO MODERATE INFLAMMTIONMETAPLASIA,MILD TO MODERATE INFLAMMTION..

..

NICOTINE STOMATITISNICOTINE STOMATITIS

MEDIAN RHOMBOID GLOSSITISMEDIAN RHOMBOID GLOSSITIS

LEUKOPLAKIALEUKOPLAKIA

NAME GIVEN BY- SCHIERMER

GREEK WORD- Leucos means white and plakia

means patch.

Definition

It is a predominantly white lesion of the oral mucosa

that cannot be characterized as any other definable

lesion ,some oral Leukoplakia’s will transform into

cancer

CLASSIFICATION

AXELL.T. et al (1996)

Homogenous

Non homogenous

Erythroplakia

ETIOLOGY

Tobacco

PATHOGENESIS

Tobacco(chemical constituents and combustion products such as tars and resins)

additional effect of heat from the burning of tobacco

+

Irritation of oral mucosa producing leukoplakic changes.

PREDISPOSING FACTORS

Alcohol

Vitamin deficiency

Candida

Viruses

CLINICAL FEATURES

Three types :

Homogenous

Nodular/Granular/Speckled/Non-homogenous

Verrucous

CLINICAL FEATURES

Age – average 60 yrs(less than 20 also recorded)

Sex – M:F = 3:2

Site – although leukoplakia can be found in any

location,buccal mucosa,gingivae and Vermillion

border of the lip are involved.Lips,palate,retro

molar area ,floor of the mouth,tongue are less

likely sites.

CLINICAL FEATURES

•Homogenous refers to a localized lesion or an

extensive white patch that presents a relatively

consistent pattern throughout ,even though the

surface of the lesion may be described variously as

corrugated(ebbing tide),with a pattern of fine

lines(cristae),wrinkled(dry-cracked mud)or

papillomatous.

CLINICAL FEATURES

Nodular leukoplakia refers to a mixed red and

white lesion with small Keratotic nodules are

scattered over an atrophic patch of mucosa

CLINICAL FEATURES

Verrucous leukoplakia is one in which the

surface is broken up by multiple papillary

projections that may also be heavily keratinized

producing a lesion that bears some resemblance

to the dorsum of the tongue.

INVESTIGATIONS

SMEAR-to rule out candidal involvement

Toludine blue application.

Biopsy

DIFFERENTIAL DIAGNOSIS

HOMOGENOUS

CANDIDAL LEUKOPLAKIA

SYPHILITIC WHITE PATCH

CRYPTOGENIC LEUKOPLAKIA

LEUKOPLAKIA INDUCED BY GALVANISM,TRAUMA,ETC.

PLAQUE TYPE LICHEN PLANUS

SPECKLED

ATROPHIC LICHEN PLANUS

MALIGNANT POTENTIAL

Over all : 3-6%

Type wise : Homogenous 0.5-1.7 %

Speckled 20%

Site wise : Floor of the mouth - highest

TREATMENT

Stop the habit

Topical anti fungal for 2 weeks

Biopsy and topical Vit A application

Beta carotene 5000 IU/day(chemo prevention)

GUIDELINES FOR MANAGEMENT

Clinical observation without biopsy is dangerous

Response to hyperkeratotic leukoplakia is

unpredictable,so biopsy to be repeated every 6 –

12 months particularly if the lesion changes in

size or physical characteristics.

Adequate follow up,especially for

nodular,Verrucous forms and leukoplakia at the

floor of the mouth and tongue.

TREATMENT(other modes)

Topical Bleomycin

Cryo surgery

Laser ablation

Surgical stripping with graft coverage

CANDIDIASISCANDIDIASIS

DEFINITION

Infection caused by fungus CANDIDA

CLASSIFICATION

Candidiasis

Primary Secondary

Acute Candida-associated lesions

chronic

ORAL CANDIDIASIS

Acute :

Chronic :

Candida associated : lesions

Pseudomembranous

Erythematous(atrophic)

Pseudomembranous

Erythematous

Plaque like

Nodular

Denture stomatitis

Angular chelitis

Median rhomboid glossitis

secondarysecondary

Familial chronic mucocutaneous candidiasis Familial chronic mucocutaneous candidiasis Diffuse chronic mucocutaneous candidiasis Diffuse chronic mucocutaneous candidiasis Candidiasis endocrinopathy syndromeCandidiasis endocrinopathy syndrome Familial mucocutaneous candidiasis Familial mucocutaneous candidiasis Severe combined immunodeficiency Severe combined immunodeficiency DiGeorge syndrome DiGeorge syndrome Chronic granulomatous disease Chronic granulomatous disease Acquired immune deficiency syndrome (AIDS)Acquired immune deficiency syndrome (AIDS)

PREDISPOSING FACTORS

Marked changes in the oral microbial flora

Broad spectrum antibiotics

Excessive use of anti microbial mouth rinses.

Xerostomia secondary to anticholinergic agents and

SG disease.

Chronic local irritants.

Dentures

Orthodontic appliances

Heavy smoking

Administration of cortico steroids

(topical,oral,inhalation & systemic)

Radiation to head and neck

Age (infancy,pregnancy,old age)

Hospitalization age, debilitating diseases,antibiotics)

PREDISPOSING FACTORS

CLINICAL FEATURESPSEUDOMEMBRANOUS CANDIDIASIS

Superficial infection of the upper layer of the

epithelium,resulting in the formation of patchy white

flecks.

Surrounding mucosa-may /may not be

reddened.Plaque removal ,by rubbing or scraping shows

erythema/shallow ulceration.

Transient episodes of thrush

may occur as isolated

prominences that disappear

spontaneously with

minimum/no treatment.

Common neonates and

children.

Typical lesion of infants-soft white or bluish

white,adherent patches on the oral mucosa at

times,extending to circum oral tissues.

Lesions are painless

Can be removed with tissue difficultly,leaving

raw bleeding surfaces.

In adults-

Lesions may evolve beneath dentures or any other area of the oral cavity.

Inflammation,erythema and painful eroded may more be more often associated with.

Entire oral mucosa may be involved.

Mild symptoms compared to other stomatitis’

Burning of mouth and throat precede in antibiotic therapy predisposed.

CHRONIC PLAQUE TYPE

CHRONIC NODULAR TYPE

DIFFERENTIAL DIAGNOSIS

Flecks of milk

Flecks of food debris

Antacids remaining on the oral mucosa ,esp. in

infants.

Debilitated elderly patient ( intern’s thrush )

Cheek biting

Chemical burn

ERYTHEMATOUS(ATROPHIC)

Includes antibiotic sore mouth.

Red pattern of raw atrophic mucosa persists with no

evidence of pseudomembranes.

Generalized depapillation of tongue.

Palate and buccal mucosa can be involved.

Pt develops symptoms of bad taste,oral burning,sore

throat during convalescent periods of illness,treated

with broad – spectrum antibiotics.

ERYTHEMATOUS(ATROPHIC)ERYTHEMATOUS(ATROPHIC)

HYPERPLASTIC CANDIDIASIS

Chronic disease

Raised lesions that vary from small,palpable,translucent areas

whitish areas to large dense opaque plaques which are hard and

rough to touch.

Homogenous/Speckled/Nodular areas which do not rub off.

3- 50 % of candida –hyperplastic.

Treatment Treatment

NystatinNystatin Cream Apply to affected area.Cream Apply to affected area.

Oral suspension, Apply after meals 4x/d, usually for Oral suspension, Apply after meals 4x/d, usually for

7 d, 100,000 U continue use for several days after 7 d, 100,000 U continue use for several days after post clinical healingpost clinical healing

Candid -BCandid -B cream cream

ASSOCIATED LESIONSCHRONIC ATROPHIC /DENTURE SORE MOUTH

AETIOLOGY

•Traumatic : Irritation is the foremost etiology.

Inadequate,ill fitting dentures,

abnormal movements

•Toxic: Chemical action of free monomer

Poor denture hygiene

Putrefaction of chemical food

•Allergic : Hypersensitivity to denture

material

•Infections : Nonspecific bacteria,

candidal species

•Malnutrition: Alcoholism, DM

(uncontrolled) Anemia's

•Idiopathic: Resistance to treatment

•Stomatitis with palatal inflammatory

hyperplasia

CLINICAL FEATURES

Palatal hyperplasia

Palatal mucosa – velvety or may resemble

an over ripe berry and bleed on slight

pressure.

Pain and burning

Intensely reddened ,glistening and slightly

swollen surfaces.

Denture StomatitisDenture Stomatitis

ANGULAR CHELITIS/STOMATITIS

Any inflammatory lesion of the corner of the mouth.

DEFINITION

AETIOLOGYMALNUTRITION

MECHANO-TOXICITY

INFECTION

TRAUMA

ALLERGY

IDIOPATHIC

CLINICAL FEATURES

Intensely red,fissured,eroded or ulcerated

areas

Generally accompanied by symptoms of

soreness,tenderness,burning or frank pain.

Malnutrition induced

•Intensely red in the muco-cutaneous

junction surrounding the skin.

•Fissures and superficial erosion on an

inflamed base

•Ulceration coated with Greyish-white

or yellow membrane or exudate.

Mechano-toxic variety

Loss of intermaxillary distance

Closure of bite,acceleration of transverse folds of skin at the angle of the mouth.

Saliva drools out at the corners

Fluids deposited leaves accentuated folds.

Drying of saliva and formation of irritating end- products

Inflammation

Infection type :

Strepto/Staphylo/Candida

Traumatic type :

Dental procedures

Allergy/toxic :

Cosmetics/lipsticks/ointments

Idiopathic :

Metabolism/Harmonal/Emotional

INVESTIGATIONSMICROBIOLOGY:

•Smear from the lesion

Grams/PAS•Swab : cotton dipped swab•Imprint culture•Saliva culture

HISTOPATHOLOGYBiopsy

IMMUNOLOGICAL TESTS

•Candida agglutination,precipitation immunoflorescence

•ELISA

HEMATOLOGY

TLC,DC,Folate,Vit B 12,Serum Ferritin

TREATMENTTopical antifungal : Clotrimazole( Azoles )

Ketaconazole :200 mg x 7 days

Fluconozole : 50 mg O.D x 10 days

Intraconozole : 100 – 200 mg/day x 2

weeks

DNA Analogues : Flucytomine

50 – 150 mg/kg/day x

quad/day(divided doses )

Amphoterecin

100 mg/ml