1. GOOD AFTERNOON
Dr.Rajesh

2. LESIONS

3. 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.

5. Papule
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.

7. Plaques
Solid raised lesions that are over 1
cm in diameter; they are large
papules.

9. Nodules
These lesions are present deep in the
dermis,and the epidermis can be
easily moved over them.

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

13. Bullae
Elevated blister like
lesions containing clear
fluid that are over 1 cm in
diameter.

15. Erosions
Moist red lesions often caused by the
rupture of vesicles or bullae as well as
trauma.

17. WHITE
LESIONS

18. 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.

19. Red Lesion
Any area of reddened mucosa that may be
smooth and atrophic looking or exhibits a
granular, velvety texture

20. Precancerous Lesions: defined as a morphologically
altered tissue in which cancer is more likely to occur.
e.g.
Leukoplakia , Erythroplakia, Actinic chelitis, Palatal
Changes 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.

21. PREMALIGNANT CONDITION IN DETAILS

ORAL SUBMUCOUS FIBROSIS

ACTINIC KERATOSIS

DYSKERATOSIS CONGENITA

XERODERMA PIGMENTOSUM

PEUTZ JEGHERS SYNDROME

TERTIARY SYPHILIS

BOWEN’S DISEASE

EROSIVE LICHEN PLANUS

DISCOID LUPUS ERYTHEMATOUS
PLUMMER VINSON SYNDROME

22. White lesions classification











HEREDITARY WHITE LESIONS
REACTIVE INFLAMATORY WHITE LESIONS
INFECTIOUS WHITE LESIONS
IDIOPATHIC TRUE LEUKOPLAKIA
BOWENS DISEASE
ORAL LICHEN PLANUS
LICHENOID REACTIONS
DEVELOPMENTAL- ECTOPIC LYMPHOID TISSUE
FORDYCES GRANULES
GINGIVAL CYSTS OF ADULT N NEW BORN
MISCELLIANEOUS

23. HEREDITARY WHITE
LESIONS




LEUKODEMA
WHITE SPONGY NEVUS
HEREDITARY BENIGN
INTRAEPITHELIAL DYSKERATOSIS
DYSKERATOSIS CONGENITA

24. REACTIVE INFLAMMATORY
WHITE LESIONS








LINEA ALBA.
FRICTIONAL KERATOSIS.
CHEEK CHEWING.
CHEMICAL INJURIES OF ORAL MUCOSA.
ACTINIC KERATOSIS.
SMOKELESS TOBACCO INDUCED KERATOSIS.
NICOTINE STOMATITIS.
SANGUINARIA INDUCED LEUKOPLAKIA

25. DEVELOPMENTAL WHITE LESIONS
—ECTOPIC LYMPHOID TISSUE
FORDYCES GRANULES
GINGIVAL CYSTS OF NEW BORN N
ADULTS.
MISSELLANEOUS LESIONS


GEOGRAPHIC TONGUE
HAIRY TONGUE

26. Lichen
Planus

27. 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.

28. TYPES
Reticular
 Annular
 Plaque(hypert
rophic)
 Papular

Erosive
 Bullous
 Atropic
 Pigmented


29. ETIOLOGY
Interplay of host,lifestyle and environmental
factors
Cell-mediated
immunity
initiated
endogenous or exogenous factors.
by

30. EXOGENOUS/ENDOGENOUS
FACTORS






Genetic
Dental materials
Drugs
Infectious agents
Auto immunity
Immunodeficiency







Food allergy
Stress
Habits
Trauma
DM & HTN
Malignancies
IBD

31. 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

32. Basal cell degeneration
Pyknotic and shrunken
basal cells(civatte
bodies)
Apoptotic cell
Phagocyotosed
Incapable of phagocytosis
Extruded into the
underlying
dermis(colloid bodies)

33. 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
violaceous hue and a fine scaly surface.
with

34. 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.

35. 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

36. 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)

37. 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

38. BULLOUS
•Rarely observed form
•Bullae and vesicles range from few mmseveral cm.,short-lived and rupture into
ulcers.
•Seen in postero-inferior aspect of the buccal
mucosa
•Striae to be seen here also.

43. 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

44. INVESTIGATIONS

HB%,CT & BT

Biopsy

Immunofluoroscence

45. IMMUNOFLUOROSCENCE
•Positive direct
Immunofluoroscence, at the level of
BM
•Pattern may be globular or linear.

46. TREATMENT
Reasons to treat:
Symptomatic cases
Malignant potential(erosive LP)

47. TREATMENT
Asymptomatic
Reassurance
Symptomatic
Treat

48. SYMPTOMATIC CASES
No Candida
Candida
Mild symptoms
Mild symptoms Severe symptoms
Topical steroid
Systemic steroid
+
+
Topical anti fungal Topical anti fungal
Symptomatic maintenance
with topical anti-fungal and
topical steroids
Topical steroid
Ulcers resistant to
heal
Add intralesional
steroids
Severe symptoms
Systemic steroid
Symptomatic
maintenance
therapy

49. TOPICAL STEROIDS
•Triamcinalone acetate 0.01%
•Clobetasol propionate
•Flucinonide

50. SYSTEMIC STEROIDS
PREDNISOLONE 20-40 mg
early morning once a day
(taper gradually)

51. OTHER MODALITIES
Topical cyclosporine rinses
Systemic azathioprine
Levamisole(immuno modulator)
Dapsone (immuno modulator)
Surgery (lasers, cryo)
Photo-chemo therapy(PUVA)
Magneto therapy
Reflexo therapy

52. EROSIVE LICHEN PLANUS
Malignant potential-2.7%
Treat with topical/systemic
vitamin A for reversal of
dysplastic changes.

54. OSMF

55. 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

56. ETIOLOGY
ARECANUT CHEWING WITH
GENETIC PREDISPOSITION

57. PATHOGENESIS
Arecanut
Arecoline(5-7%)
Tannins(11-26%)
Alkaloids(0.15-0.6%)
Fibroblast
proliferation
Stimulates collagen
synthesis
Collagen fibrils resistant to
human collagenase

58. PATHOGENESIS
ARECANUT
ARECANUT CHEWING
OSMF
MUSCLE
CONTRACTION
JUXTA EPITHELIAL
HYALINIZATION
VASO OBLITERATION
DIMINISHED BLOOD
SUPPLY
OVER ACTIVITY
GLYCOGEN DEPLETION
MUSCLE FATIGUE AND DEGENERATION
FIBROSIS AND SCARRING OF THE MUSCLE

59. CLINICAL FEATURES
•Any age - 20 – 60 yrs predominantly
•Male predominance

60. 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.

61. •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

62. SIGNS
•Blanching
appearance
,which
to
the
imparts
oral
Marble-like
mucosa.May
be
localized,diffused or lace -like network.
•As disease progresses mucosa becomes stiff and
vertical fibrous bands appear.

63. 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.

64. •Tonsils- may be pressed between the faucial
pillars.
•Soft palate -Mobility is restricted when is
involved.
•Uvula-shrunken
appearance
bud like or hockey stick

65. •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.

68. 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

69. Functional staging
•A –mouth opening >20mm
•B-mouth opening 11-19 mm
•C-mouth opening < 10 mm

70. INVESTIGATIONS
•Increased ESR
•Anemia
•Eosinophilia
•Increased IgG
•Decreased serum iron
•Increased total Fe binding capacity
•Decreased total saturation of transferrin
•Decreased total serum iron

71. Treatment
Elimination of the habit
Nutritional support
Bland diet
Cases without bands-topical corticosteroids
Cases with bands-intra-lesional corticosteroids
Physiotherapy
Retinoids

72. TREATMENT MODALITIES
Intra lesional - cortico steroids
Intra lesional - cortico steroids with hyalurinadase
Systemic – Levamisole/Dapsone
Soft lasers
Turmeric oil
Homeopathy(calcaria florica)

73. 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

74. ACITINIC(SOLAR)
KERATOSIS/ELASTOSIS /
CHELITIS

75. DEFINITION
IS A PREMALIGNANT SQUAMOUS
CELL LESION DUE TO LONG TERM
EXPOSURE TO SOLAR RADIATION.

76. 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%)

78. TREATMENT
Topical 5-fluoro uracil
Surgical lip shaving
procedures
Topical steroids in
between treatments to
control lip swelling

79. LEUKOEDEMA

80. 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

82. LINEA
ALBA
BUCCALIS

83. 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.

85. FORDYCE’S
GRANULES

86. FORDYCE’S GRANULES

87. Ectopic presence of tubulo-acinar sebaceous glands in
oral cavity.
Appears in 80-90 % of adult population.
Appears
plaques.
as
small
,white/yellowish
sub-mucosal

88. Seen on Vermillion border, buccal mucosa,
occasionally on the palate , gingiva and the
tongue.
No specific function/does not increase with
age.
Occasionally
transforms
cyst/sebaceous adenoma.
into
pseudo

89. WHITE SPONGY NEVUS

Etiopathogenesis : Mutations in
Genes Coding For
Epihtelial Keratin Of Type K4 N K33.

:Clinical features:

Age:18 –22yrs….

M=f.Autosomal Dominant Disorder….

Site : Buccal Mucosa.

Extra Oral Sites : Oesophagus,anogenital Mucosa.

.Management: No Specific Treatment Required.

90. WHITE SPONGY NEVUS

91. NICOTINE STOMATITIS

ETIOLOGY: HEAVY CIGARETTE ,PIPE ,CIGAR SMOKING.

C/F:NUMEROUS ELEVATED PAPULES WITH RED PUNCTATED
CENTER…… INFLAMMED SALIVARY GLAND WITH ALTERED
DUCTS.

HISTOPATH:HYPERKERATOSIS,SQUAMOUS
METAPLASIA,MILD TO MODERATE INFLAMMTION.
.

92. NICOTINE STOMATITIS

93. MEDIAN RHOMBOID GLOSSITIS

94. LEUKOPLAKIA

95. NAME GIVEN BYSCHIERMER
GREEK WORD- Leucos
means patch.
means white and plakia

96. 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

97. CLASSIFICATION
AXELL.T. et al (1996)
Homogenous
Non homogenous
Erythroplakia

98. ETIOLOGY
Tobacco

99. 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.

100. PREDISPOSING FACTORS
Alcohol
Vitamin deficiency
Candida
Viruses

101. CLINICAL FEATURES
Three types :
Homogenous
Nodular/Granular/Speckled/Non-homogenous
Verrucous

102. 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.

103. 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.

104. CLINICAL FEATURES
Nodular leukoplakia refers to a mixed red and
white lesion with small Keratotic nodules are
scattered over an atrophic patch of mucosa

105. 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.

111. INVESTIGATIONS
SMEAR-to rule out candidal involvement
Toludine blue application.
Biopsy

112. DIFFERENTIAL DIAGNOSIS
HOMOGENOUS
CANDIDAL LEUKOPLAKIA
SYPHILITIC WHITE PATCH
CRYPTOGENIC LEUKOPLAKIA
LEUKOPLAKIA INDUCED BY GALVANISM,TRAUMA,ETC.
PLAQUE TYPE LICHEN PLANUS
SPECKLED
ATROPHIC LICHEN PLANUS

113. MALIGNANT POTENTIAL
Over all : 3-6%
Type wise : Homogenous 0.5-1.7 %
Speckled
20%
Site wise : Floor of the mouth - highest

114. TREATMENT
Stop the habit
Topical anti fungal for 2 weeks
Biopsy and topical Vit A application
Beta carotene 5000 IU/day(chemo
prevention)

115. 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.

116. TREATMENT(other modes)
Topical Bleomycin
Cryo surgery
Laser ablation
Surgical stripping with graft
coverage

117. CANDIDIASIS

118. DEFINITION
Infection caused by fungus CANDIDA

119. CLASSIFICATION
Candidiasis
Secondary
Primary
Acute
chronic
Candidaassociated
lesions

120. ORAL CANDIDIASIS
Acute :
Pseudomembranous
Erythematous(atrophic)
Chronic :
Pseudomembranous
Erythematous
Plaque like
Nodular
Candida associated :
lesions
Denture stomatitis
Angular chelitis
Median rhomboid
glossitis

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

122. 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.

123. Chronic local irritants.
Dentures
Orthodontic appliances
Heavy smoking

124. PREDISPOSING FACTORS
Administration of cortico steroids
(topical,oral,inhalation & systemic)
Radiation to head and neck
Age (infancy,pregnancy,old age)
Hospitalization age, debilitating diseases,antibiotics)

125. CLINICAL FEATURES
PSEUDOMEMBRANOUS 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.

126. Transient episodes of thrush may occur as
isolated prominences that disappear
spontaneously with minimum/no
treatment.
Common neonates and children.

127. 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.

128. 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.

130. CHRONIC PLAQUE TYPE

131. CHRONIC NODULAR TYPE

132. 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

133. 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.

134. ERYTHEMATOUS(ATROPHIC)

135. 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.

136. Treatment

Nystatin

Cream Apply to affected area.

Oral suspension, Apply after meals 4x/d, usually for 7
d, 100,000 U continue use for several days after post
clinical healing
Candid -B cream


137. ASSOCIATED LESIONS
CHRONIC ATROPHIC /
DENTURE SORE MOUTH

138. 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

139. •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

140. 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

141. Denture Stomatitis

142. ANGULAR
CHELITIS/STOMATITIS

143. DEFINITION
Any inflammatory lesion of
the corner of the mouth.

144. AETIOLOGY
MALNUTRITION
MECHANO-TOXICITY
INFECTION
TRAUMA
ALLERGY
IDIOPATHIC

145. CLINICAL FEATURES
Intensely red,fissured,eroded or ulcerated
areas
Generally accompanied by symptoms of
soreness,tenderness,burning or frank pain.

147. 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.

148. 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

149. Infection type
:
Strepto/Staphylo/Candida
Traumatic type :
Dental procedures
Allergy/toxic
:
Cosmetics/lipsticks/ointments
Idiopathic
:
Metabolism/Harmonal/Emotional

150. INVESTIGATIONS
MICROBIOLOGY:
•Smear from the lesion
Grams/PAS
•Swab : cotton dipped swab
•Imprint culture
•Saliva culture
HISTOPATHOLOGY
Biopsy
IMMUNOLOGICAL TESTS
•Candida agglutination,precipitation immunoflorescence
•ELISA
HEMATOLOGY
TLC,DC,Folate,Vit B 12,Serum Ferritin

151. TREATMENT
Topical 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