This document provides an overview of oral mucosal lesions, including their classification, characteristics, diagnosis and treatment. It discusses common lesions like oral candidiasis, oral hairy leukoplakia, oral leukoplakia and erythroplakia. It describes premalignant conditions such as oral submucous fibrosis. Signs, symptoms and histopathological features of each condition are outlined. The document also reviews diagnostic approaches and various treatment options for each oral mucosal lesion.

1. Oral Mucosal Lesions
Presented by: Dibya Falgoon Sarkar (Dept. of Oral & Maxillofacial Surgery)

2. Contents
According to Burket oral mucosal lesions can be
broadly classified into:
 Red and white lesions
 Pigmented lesions
 Ulcerative, vesiculous and bullous lesions

3. Red and white lesions
 Infectious diseases:
1. Oral candidiasis
2. Oral hairy leukoplakia
 Premalignant disorders:
1. Oral leukoplakia and
erythroplakia
2. Oral submucous fibrosis
 Immunopathologic diseases:
1. Oral lichen planus
2. Lichenoid reactions
3. Lupus erythematosus
 Toxic reactions:
1. Tobacco pouch keratosis
2. Nicotinic stomatitis
 Reactions to mechanical
trauma:
1. Morsicatio
2. Frictional keratosis
 Others:
1. Benign migratory glossitis
2. Leukoedema
3. White sponge nevus

4. Oral Candidiasis (Thrush)
 Usually caused by the normally present Candida albicans which
becomes pathogenic because of altered host defense system.
Systemic factors Local factors
Diabetes , advanced systemic
disease
Use of dentures
Xerostomia- Drugs or radiation Reduced vertical dimension
Sjogren syndrome Overuse of antibiotic
mouthrinses
HIV infection & AIDS Lip-licking habit
Systemic antibiotic,
corticosteroid therapy

5. Classification of oral candidiasis
Primary oral candidiasis Secondary oral candidiasis
Pseudomembranous HIV-AIDS
Erythematous Familial chronic
mucocutaneous disease
Chronic plaque like DiGeorge syndrome
Denture stomatitis Candidiasis endocrinopathy
syndrome
Angular chelitis
Median rhomboid glossitis
Hyperplastic

6. Clinical presentations of oral candidiasis
Angular cheilitis Median rhomboid glossitis
Denture stomatitis HyperplasticPseudomembranous
Erythematous

7. Differential diagnosis
 Leukoplakia- A leukoplakia will always remain adherent to the
mucosa on rubbing. Candidiasis generally presents as
pseudomembrane
 Oral lichen planus- Generally presents as a reticular
striae(Wickham’s striae) and is adherent on rubbling. Often presents
with a burning sensation
 Secondary syphilis- Generally associated with a primary chancre
over site of inoculation
 Chemical/ heat burns

8. Diagnosis and treatment
 Investigation- Tissue biopsy stained with PAS stain/ KOH mount, Fungal
culture
 Treatment-(according to Marx & Stern)
1. Mild forms: Clotrimazole oral solution 5ml 3-4times daily for 2 weeks
2. Chronic well established: Nystatin oral suspension (1lacU/ml, 5ml, 4 times
daily) along with Clotrimazole troches (10mg, 5times daily)
Refractory forms : Fluconazoles (100mg capsules once daily, 2 weeks)
3. Disseminated forms: Amphotericin B i.v. with D5 solution at a rate of 0.2-0.7
mg/kg/day. But it can lead to nephrotoxicity

9. Oral hairy leukoplakia
 Oral hairy leukoplakia is the second
most common HIV-associated oral
mucosal lesion
 Associated with low CD4 T– lymphocyte
count
 Etiology- Epstein-Barr virus
 Prevalance- Prior to HAART era it was
around 25%
In AIDS patients it is around 80%
 Male> Female
 Prevalent in smokers

10. Clinical features, Diagnosis,
Treatment
 Site predilection- Lateral
borders of tongue
 Vertical white folds which
cannot be scraped off
 Asymptomatic condition
 Diagnosis- Biopsy
 Treatment- Antiviral
medication

11. Premalignant disorders
 Premalignant lesions:
 Oral leukoplakia
 Erythroplakia
 Reverse smoker’s palate
 Premalignant conditions:
 Oral submucous fibrosis
 Oral lichen planus

12. Oral leukoplakia
 Oral leukoplakia is defined as a white plaque of questionable risk having
excluded other known diseases or disorders that carry no risk for cancer
 Etiology: Smoking, use of tobacco products, alcohol abuse which cause genetic
changes in the oral mucosa
 Prevalence- 2.6%
 Mean age- 30-50 years
 Sex predilection: Men > Women
 Found in all oral sites. High-risk sites for
malignant transformation:
1. Floor of Mouth
2. Lateral borders of tongue

13. Types of oral leukoplakia
Homogenous Nonhomogeneous
White, well-demarcated plaque with identical
pattern throughout the entire lesion
• Presents as patches/plaques intermingled
with red elements
• Often termed as erythroleukoplakia/ speckled
leukoplakia
• Increased chances of malignant
transformation

14. Classification and Staging of Oral
Leukoplakia
Van der Waal et al., Journal of Oral oncology (2000)
 L (size of leukoplakia)
 L1: Size of single/ multiple leukoplakias together ≤ 2cm
 L2: Size of single/ multiple leukoplakias together 2-4cm
 L3: Size of single/ multiple leukoplakias together ≥4cm
 P (pathology)
 P0: No epithelial dysplasia
 P1: Distinct epithelial dysplasia present
 Staging:
 Stage I: L1Po
 Stage II: L2Po
 Stage III: L3Po or L1/L2P1
 Stage IV: L3P1

15. Management of oral leukoplakia
 Prognosis of leukoplakia patients is decided by:
1. Size of lesion
2. Homogeneous/non-homogeneous pattern
 According to Burket, lesions <200sq.mm shows better prognosis
 Cryotherapy can be used by it has limitations with depth control
 Laser surgery and fulguration is widely used to eradicate
leukoplakia and erythroplakia but tissue specimen for biopsy is
not available.
 According to Marx & Stern, leukoplakias which are graded as
moderately dysplastic/ carcinoma in-situ are managed with
surgical excision with 1cm margin regardless of size

16. According to van der Waal et al
Provisional clinical diagnosis
of leukoplakia
Elimination of possible cause
(2-4 weeks observation)
No possible cause
(Definitive clinical diagnosis)
Good response
No response
(Definitive clinical diagnosis) Biopsy
Definable lesion
• Management
accordingly
No definable lesion
Dysplasia/No dysplasia
Definable lesion
• Management
accordingly
• Treatment/ Observation
• Follow-up

17. Proliferative verrucous leukoplakia
 PVL is a field cancer phenomenon by which clinically normal-appearing oral
mucosa slowly transforms through advancing stages of clinical leukoplakia,
verrucous hyperplasia/ carcinoma, and then into invasive SCC
 More common in older women(4:1)
 Lower gingiva is a predilection site
 Most patients(78%) are usually non smokers
 High recurrence rate
 High malignant potential
 Increased correlation with oral Candida
infection

18. Diagnostic work-up &
Management of PVL
 Diagnosis mainly dependent on biopsy
 Principles of PVL excisions differ from other leukoplakias:
1. Clear all peripheral margins
2. Areas of excision often cover large surfaces and thus split-
thickness skin graft may be necessary after excision
 Chemoprevention with fluconazole oral suspension and
selenium(100microgram daily)
 Literature shows bad prognosis in laser treated PVL cases

19. Erythroplakia
 The term erythroplakia is used analogously to
designate lesions of oral mucosa that present
as red areas and cannot be diagnosed as any
other definable lesions (WHO, 1994)
 Rare premalignant lesion with a prevalence of
0.09% (Acc. to Shafer & Waldron)
 Age predilection: 6th-7th decades of life
 Male: Female - 1:1
 Site: Common in soft palate, buccal mucosa
and floor-of-mouth
 Aetiology: Same as those associated with
squamous cell carcinoma

20. Erythroplakia
 Rare lesion with a malignant
transformation rate of 26.3%
(Acc. To Reddi & Shafer’s study)
 Treatment : Observation for 1-2
weeks following elimination of
irritants. Complete excision of
the lesion with clear margins
down to the submucosal level is
the treatment of choice
 Recurrence rate <5% (Acc. To
Burket)
Differential diagnosis of red lesions of
oral mucosa:
1. Mycotic infections
• Erythematous candidiasis
• Denture stomatitis
• Histoplasmosis
2. Bacterial infections
• Tuberculosis
3. Mucosal diseases
• Pemphigus, pemphigoid
• Atrophic lichen planus
• SLE
4. Others
• Kaposi sarcoma
• Haemangioma
• Amelanotic melanoma

21. Oral submucous fibrosis
 Oral submucous fibrosis (OSF) is a collagen disorder commonly
seen in the Indian subcontinent
 First described by Schwartz in 1952
 Pindborg et al. found a prevalence of 0.2~0.5% in India
 Sex predilection: 5% prevalence in women & 2% in men
 Areca nut (the fruit of the Areca catechu) commonly known as
betel nut or supari, plays a crucial dual role in the etiology of OSMF
 The attendant trismus is a result of juxtaepithelial hyalinization and
secondary muscle involvement (i.e., muscular degeneration and
fibrosis)
 Malignant transformation has been noticed in 3-7.6% of cases

22. Pathogenesis of OSMF
Areca nut
Arecoline
(5-7%)
Tannins
(11-26%)
Alkaloids
(0.15%-0.6%)
Fibroblast
proliferation
Stimulates collagen
synthesis
Collagen fibrils resistant
to collagenase

23. Clinical features and staging
 One of the following characteristic must
be present :
1. Palpable fibrous bands
2. Mucosal texture feels tough and
leathery
3. Blanching of mucosa together with
histologic features consistent with
OSMF
4. Differential diagnosis: Scleroderma
(Widening of PDL spaces present along
with skin manifestations)

24. According to Khanna-Andrade article
Stage Clinical features Histology
Group I • The common initial
symptom was a burning
sensation in the mouth.
• Excessive salivation
• The mouth opening was
normal in all cases.
• fine fibrillar collagen
network was seen to be
interspersed with marked
edema. Blood vessels were
dilated and congested
• epithelium was essentially
normal and
nonkeratinized, with
occasionally some hy-
perplasia
Group II • Interincisal openings of
26-35 mm.
• The soft palate and faucial
pillars were the areas
primarily affected. The
buccal mucosa ap- peared
mottled and marble-like
• Juxtaepithelial hyalini-
zation was seen with the
collagen present as
thickened but separate
bundles.
• Flattening or shortening of
the epithelial rete pegs
was evident with varying
degrees of keratinization

25. Stage Clinical features Histology
Group III: moderately advanced
cases
• Trismus was evident, with an
inter- incisal opening of 15-
25 mm
• Vertical fibrous bands could
be palpated in the premolar
area.
• Juxtaepithelial hyalini- zation
was present. Thickened
collagen bundles were
faintly discernible, separated
by very slight, residual
edema
• Muscle fibers were seen to
be interspersed with
thickened and dense
collagen fibers.
Group IVa • Trismus was severe with an
interincisal opening of 2-15
mm.
• The fauces was thickened,
shortened, and firm to
palpation, with the tonsils
compressed between the
fibrosed pillars.
• Shrunken uvula
Collagen was hyalinized as a
smooth sheet eliminating all
evidence of individual bundles.
Extensive fibrosis had
obliterated the mucosal blood
vessels and eliminated the
melanocytes, a feature which
explained the clinically
observable loss of pigmentation
Group IVb • advanced cases with
premalignant and malignant
changes

26. Management of OSMF
 Actively discourage patients from
consuming areca nut and other
chronic irritants such as hot and spicy
foods
 Well balanced diet with vitamin A &
B-complex substitutes
 Wherever possible we extract the
third molars
 Group I & II patients are put on
conservative therapy and active
physiotherapy
 Group III & IV patients are treated by
surgical intervention

27. Conservative therapy in OSMF
 Physical therapy:
1. Physical exercise
2. Microwave diathermy
 Medical therapy:
 Modulators of inflammation:
1. Corticosteroid
2. Interferon gamma
3. Placental extracts
 Modulators for vascularity:
1. Pentoxiphylline
2. Nylidrin
 Fibrinolysis:
1. Hyaluronidase
2. Collagenase
 Nutritional support and
antioxidants:
1. Beta-carotene
2. Lycopene
3. Vitamins
 Ayurvedic treatment:
 Turmeric
 Tea pigments

28. Conservative therapy in OSMF
 Corticosteroid therapy: Submucosal injections of triamcinolone
acetonide (40 mg) injected into the faucial pillars, retromolar area,
and buccal mucosa. On average, a dose of 150-200 mg of local
submucosal corticosteroid injection was given in divided doses at
10-day intervals for a period of 2-3 months.
 Hyaluronidase(1500 I.U)- 0.5ml injected intralesionally twice a
week for 10 days
 Placental extract (Placentrex)- 2ml intralesional once a week
along with iodine and vitamin B complex

29. Surgical management
 Rationale: Incision or surgical release of fibrous bands followed by forceful
opening of mouth, and covering the surgical defects using various flaps
and biosynthetic materials
 In some cases we may need temporalis myotomy and bilateral
coronoidectomy
Extraoral flaps Intraoral flaps Microvascular Alloplasts
Split thickness
skin grafts
Tongue flap ALT flap Collagen
membrane
Temporalis
muscle/ fascia
pedicled flap
Palatal island flap Radial forearm
free flap
Artificial dermis
Nasolabial flap Buccal fat pad
Amnion graft

30. Review of literature
 Khanna & Andrade found disappointing results with split thickness
skin grafting as they found marked shrinkage. They advocated
bilateral palatal flaps.
 Borle & Borle also encountered disappointing results with skin
grafts. They used tongue flaps. But OSF patients show tongue
involvement in 38% cases and post op morbidities are more with
tongue flaps
 Andrade et al. and Mehrotra et al. concluded that nasolabial flaps
cannot extend adequately to cover the raw area and they also cause
facial scars
 Yeh et al. used pedicled buccal fat pad as it provided excellent
function without deteriorating esthetics

31. Verrucous carcinoma
 Verrucous carcinoma is a distinct low grade
variant of squamous cell carcinoma of oral
cavity
(According to Oral & maxillofacial surgery clinics-
2006)
 First identified by Ackerman in 1948.
 Rare tumor representing 3-4% of all oral
carcinomas
 Etiology- High incidence associated with use of
tobacco products
 16-51% of oral VCs are found in persons
without tobacco habits
 HPV is thought to be one of the causative agent

32. Clinical presentation of verrucous
carcinoma (VC)
 True VCs are slow-growing, painless,
broad-based wart-like papillary lesion
 Site: buccal mucosa (60% cases), Gingiva
(30%)
 Male predilection seen
 Age: Older than 50 years
 Shows high propensity of local invasion
rather than metastatic spread
 Evidence of osseous invasion has been
found
 Inflammatory regional lymph nodes
may be seen in some cases

33. Treatment of Verrucous
Carcinomas
 Excision to a depth of full thickness of mucosa is the treatment of choice
for oral VCs
 According to Marx & Stern excisional depth:
1. Buccal mucosa: Upto buccinator fascia
2. Gingiva: Upto a supraperiosteal plane
3. Posterior and floor of mouth lesions are excised with a 2cm margin
 Unlike squamous cell carcinomas VCs shows less radiosensitivity
 Transformation of VCs into SCCs have been seen after radiation therapy
 Recurrance rate: 26-57%

34. Oral lichen planus (OLP)
 Lichen planus is a T-cell mediated
autoimmune interface disease in
which the basal cell layer of
mucosa and/or skin is attacked
 Prevalence varies from 0.5-2.2%
 Women more commonly affected
 Mean age at the time of
diagnosis: Approx. 55yrs
 Premalignant condition
 Malignant transformation
potential 0.3-3%
 Cutaneous lesions: 15% cases

35. Clinical types of OLP
 Reticular type:
 Characterised by Wickham’s
striae of lacy, white interlacing
lines
 Most common in buccal mucosa
 Asymptomatic
 Papular type: Clinically
characterised by small white
dots which intermingle with the
reticular pattern
 Plaque type: Homogeneous
well-demarcated white plaque,
asymptomatic

36. Clinical types of OLP
 Erosive/atrophic type:
 Characterised by intense pain and
mucosal inflammation
 Presents as desquamative
gingivitis
 Ulcerative type:
 Most disabling form of OLP
 Fibrin coated ulcers surrounded
by erythematous zones and white
striae in periphery
 Bullous type: Presents as bullous
lesions surrounded by Wickham’s
striae

37. WHO diagnostic criteria for OLP (1978)
 Clinical criteria
1. Presence of white papules, anular, reticular, plaque-like lesions,
gray-white lines radiating from the papules
2. Presence of a lace-like network of slightly raised gray-white lines
(reticular type)
3. Presence of atrophic lesions with/without erosions may also have
bulla

38. WHO diagnostic criteria for OLP (1978)
 Histologic criteria
1. Presence of thickened orthokeratinised/ parakeratinised layers in
sites that are normally keratinised
2. Presence of Civatte bodies in basal layer, epithelium and superficial
part of connective tissue
3. Presence of a band-like zone of cellular infiltration in the superficial
connective tissue, consisting mainly lymphocytes
4. Signs of liquefaction degeneration in basal layer

39. Differential Diagnosis of OLP
 Papules/ reticular components have to
be present in order to establish correct
clinical diagnosis
 Differential diagnosis:
1. Discoid lupus erythematosus: Presents
with hyperkeratinisation, striae abruptly
terminate against a sharp demarcation
2. Pemphigus: Ulcerative type OLP have
same presentation
3. Leukoplakia
4. Oral candidiasis

40. Management of OLP
 Reticular and plaque forms do not require treatment other than
reassurance and follow-up
 Milder forms of erosive type are managed with topical
corticosteroids like clobetasol propionate/1% triamcinolone paste
 Topical application of cyclosporine, tacrolimus and retinoids have
been suggested as second-line of treatment
 Systematic corticosteroid therapy with oral prednisolone may be
used in extensive cases. But steroids have their side-effects
Short-term effects Long term effects
Hypertension, hyperglycaemia,
infections, peptic ulcer,
hypernatremia
Muscle wasting, delayed wound
healing, osteoporosis, cataracts

41. Systemic corticosteroid therapy protocols
Regimen I Regimen II Regimen IIIA Regimen IIIB
Oral Prednisolone
1.5mg/kg/day for 2
weeks followed by
tapering by 20mg/day
each week until a 20mg
/day dose is reached.
The dose is followed for
1month followed by
10mg/day for 3 months,
followed by 5mg every
other day for 6 months
Oral prednisolone 100-
120 mg/ day for 2
weeks after which the
drug is stopped
abruptly
• Disadv: Frequent
exacerbations
Oral prednisolone 100-
120 mg/ day for 2
weeks
• A tapering schedule
reduces prednisone
by 20mg/day each
week until lowest
possible level is
reached without
exacerbating the
disease
• Resistant
pemphigus cases
Oral prednisolone 100-
120 mg/ day for 2
weeks
• A tapering schedule
reduces prednisone
by 20mg/day each
week until a level is
reached at which
the disease is
exacerbated
• Combined with
other
immunosuppressive
drugs to reduce side
effects
Preferred in Steven
Johnson syndrome
Useful in patients with
life long steroid need
Useful regimen in
patients who cannot
tolerate high dose
steroids

42. Drug-induced Lichenoid Reactions
 Lichenoid reactions represent a family of lesions
with different etiologies with a common clinical
and histologic appearance
 Etiology and pathogenesis: DILRs resemble a
delayed hypersensitivity reaction where the
drugs and their metabolites have the capability
to act as haptens and trigger lichenoid reactions
 Clinically appears similar to cutaneous LP and
may be pruritic
 DILRs are not life-threatening like Toxic
epidermal necrolysis
Common drugs
ACE inhibitors
Antimalarials
Penicillin group
Gold and heavy metals
Sulphonamides
OHA and OCPs
Rifampicin

43. Drug-induced Lichenoid
Reactions
 Management of drug-induced lichenoid reactions:
 Discontinuation of the drug and symptomatic treatment with topical
steroids
 Patients must be cautioned of future use of same drugs

44. Systemic Lupus Erythematous
 SLE is an autoimmune disorder in which antigen-
antibody complexes become entrapped in the
capillaries of most organs. These complexes initiate
the complement cascade and inflammation
 Marked female predilection (90%) seen
 Peak incidences between 20-40 years
 Most characteristic signs-
1. Malar butterfly rash
2. Positive serum ANA test
 Pathogenesis: Development of autoantibodies
against native double stranded DNA. There marked
depletion of complement proteins

45. ACR diagnostic criteria for SLE
1. Serositis
2. Oral ulcers
3. Arthritis
4. Photosensitivity
5. Blood disorders- Lymphopenia, leukopenia, thrombocytopenia
6. Renal disorders- 0.5g/2h protonectin, cellular casts in urine
7. Anti-nuclear antibody positivity
8. Immunologic disorders
9. Neurologic disorders- seizure, psychosis
10. Malar rash
11. Discoid rash
 At least 4 of these 11 criteria must be present before definitive diagnosis of SLE can be
made along with a positive serum ANA test
 Oral ulcers are red shallow ulcers commonly found in palate and marginal gingiva

46. Differential diagnosis of SLE
1. Erythema multiforme
2. Discoid lupus erythematosus
3. Rheumatoid arthritis
4. Drug-induced lupus syndrome:
 Males are equally affected
 No neurologic/renal components
 Anti- native DNA antibodies not
present
 Symptoms improve on stoppage of the
drug

47. Treatment of SLE
 Mild forms of SLE are managed by supportive care.
NSAIDS are given in mild flare-ups. Hydroxychloroquine 400mg orally
is used to alleviate symptoms
 Severe forms with multi-organ involvement are managed with
systemic prednisone( systemic corticosteroid therapy IIIA & IIIB)
Mycophenolate and cyclophosphamide may be added to these
regimen to reduce the steroid requirement.

48. Topical therapy for Oral lesions of
SLE
Drugs Direction for use
0.05% Clobetasol gel Place on affected area(s) 2 times/ day
for 2 weeks
Triamcinolone acetonide 5mg/ml Intralesional injection
Topical clotrimazole troches (10mg) Dissolve in mouth 5 times/day for 10
days
Chlorhexidine rinse (0.12%) Swish and spit 10ml twice daily until
lesions resolve
Adapted from Brennan et al.

49. Discoid lupus erythematosus
 Also known as chronic cutaneous lupus
erythematosus
 Immune-based disease primarily targets skin and to
lesser degree, mucosa.
 Lesions show similar characteristics and site
predilection like that of SLE
 Differential diagnosis:
1. SLE (No ANAs, hypocomplementia found)
2. Psoriasis 3. Skin TB 4. Leprosy
 Treatment: Topical corticosteroids and preventive
measures are taken in mild forms
Severe forms are treated with systemic steroid
regimens I & II

50. Nicotinic stomatitis/ Smoker’s palate
 Smoker’s palate initially presents as
erythematous irritation and later transforms into
a whitish palatal mucosa reflecting a
hyperkeratosis
 Reds dot can be observed representing inflamed
orifices of accessory salivary gland ducts which
can be enlarged and metplastic
 Etiology and pathogenesis:
 Seen in cigar and pipe smokers but not in
cigarette smokers
 Caused due to a combined effect of heat and
tobacco products,
 Not a premalignant lesion
 Treatment: Cessation of smoking

51. Leukoedema
 Leukoedema is a white and veil-
like alteration of the oral mucosa
 Asymptomatic condition with no
malignant potential
 Etiology is not clear
 Unlike leukoplakia, it is more
diffuse and temporarily
disappears on stretching
 Requires no treatment

52. White sponge nevus
 Rare autosomal dominant disorder
 Caused due to mutation of genes coding for
epithelial keratin formation
 Clinical features:
• White lesions with elevated and irregular surface
• Commonly seen in buccal mucosa
 Histologically spinous epithelial cells show
marked intracellular edema and are nondysplastic
 Management: Benign, asymptomatic

53. Benign Migratory Glossitis/
Geographic tongue
 Annular lesion affecting the dorsum and margins of
tongue
 Unknown etiology, equal gender distribution
 Prevalence 1-2.5% of all oral lesions
 Clinical features:
 Circumferentially migrating lesions with erythematous
areas of depapillated tongue
 Peripheral zones are white and elevated
 Aggravates in periods of stress
 Mostly asymptomatic
 Self healing lesions
 Symptomatic patients are given topical anesthetics

54. Pigmented lesions of oral mucosa
 Hairy tongue
 Malignant melanoma
 Haemochromatosis
 Peutz-Jegher’s syndrome
 Melasma
 Amalgam tattoos
 Endogenous pigmentation

55. Hairy tongue
 Etiology is unkown in most cases
 Probable causes are:
1. Poor oral hygiene
2. Use of antibiotics/ immunosuppressant drugs
3. Therapeutic radiation
4. Excessive alcohol consumption
5. Smoking habits
 Clinically presents as an impaired desquamation of the
filiform papilla which leads to elongated papilla over dorsum
of tongue
 Pigmentation mainly comes from the oral microflora
 Patients experience physical discomfort
 Treatment: Use of tongue scrappers

56. Malignant melanoma
 Melanomas comprise of a rare group of aggressive, malignant
neoplasms which are mainly found in skin of white people
 Oral mucosal melanomas comprise of 0.2-8% of all melanomas
diagnosed, commonly found in males more than 45 years age
 Metastasis is predominantly via haematogenous routes
 Site: Most common site is palate followed by the maxillary
gingiva
Nevus Melanoma
Symmetry Asymmetry
Borders regular Irregular borders
Uniform color Color variegation
Diameter static Diameter enlargement (>6mm)
Color stable Evolution to darker pigment

57. Clinical types of Oral Melanomas
Superficial spreading
• Most common
between 40-60 years
age
• Initiallly looks like a
nevus but later
develop irregular
border and odd
shape
• This radial growth
pattern later changes
Acral lentiginous
• Rarely found in oral
cavity
• Characterised by a
flat papular lesion
with areas of
nodularity (Vertical
component
Nodular melanoma
• Most common between
50-70 years of age
• Common in men
• Shows vertical growth
• Poor prognosis
• Occasionally present as
a flesh colored
mass,amelanotic
melanoma

58. Breslow’s measurement of tumor
thickness
Thickness (mm) Risk of recurrence
<0.76 Low risk
0.76-1.50 Low to intermediate risk
1.51-3.99 Intermediate to high risk
>4.00 High risk
Indicators of poor prognosis:
• Surface ulceration
• High mitotic index
• Absence of lymphocyte infiltrations
• Distant/ regional metastasis
 Five year survival rate in patients with metastatic
melanoma is <15%

59. Treatment of oral melanomas
 According to Marx & Stern wide local excision with 3-5cm margins is
the treatment of choice. Neck dissection is to be done in cases with
cervical lymph node metastasis
 According to Burket adjuvant chemotherapy with alpha 2B interferon is
approved in cutaneous melanoma cases with >4mm thickness
 Use of adjuvant radiotherapy is a matter of debate
 8 years survival rate is about 20%
 Lungs is the most common site of metastasis followed by skin

60. Oral Mucosal Lesions- Part II
Presented by: Dibya Falgoon Sarkar (Dept. of Oral & Maxillofacial Surgery)

61. Ulcerative, vesicular and bullous lesions
Frequently used terms
1. Vesicles Small blisters containing clear fluid that are less
than 1cm in diameter
2.Bullae Elevated blisters > 1cm in diameter
3. Erosions Red lesions caused by rupture of vesicles/bullae or
by thinning of the skin
4. Ulcers A well-circumscribed, depressed lesion with an
epithelial defect
5. Pustules Blisters containing yellowish purulent matter
6. Papules Lesions raised above skin/ mucosa < 1cm in
diameter
7. Plaques Raised lesions > 1cm in diameter

62.  We can broadly divide these type of lesions into:
1. Acute multiple ulcers:
• Herpes simplex virus
• Varicella-zoster
• Erythema multiforme
• Stevens- Johnson syndrome & Lyell disease
• Necrotizing ulcerative gingivitis & periodontitis
2. Recurring oral ulcers:
• Recurrent apthous stomatis
• Behcet syndrome
3. Chronic multiple ulcers:
• Pemphigus vulgaris
• Pemphigoid
4.Single ulcers: mostly traumatic ulcers
Ulcerative, vesicular and bullous lesions

63. Herpes simplex virus infections (HSV)
 HSV infections are caused by the Herpesviridae family.
Spreads via airborne/ direct contact.
 In general, infections above the waist are caused by HSV-
1 and below waist by HSV-2
 Pathogenesis: Primary lesion is caused by inoculation of
the virus in the oral mucosa, skin and eye with infected
secretions
 The virus then travels along the sensory neurons and
causes a chronic, latent infection in sensory ganglion
 Recurrent herpes occurs when HSV reactivates at latent
sites and travels centripetally to the mucosa/ skin

64. Clinical manifestations
of HSV infection
 Primary herpetic gingivostomatitis:
• Caused mostly in children and young adults
• Painful vesicular lesions on mucosal surfaces
• Febrile, cervical lymphadenopathy
• Lasts for 10 days and resolve on its own
 Herpetic whitlow:
• Occupational hazard among dentists
• Contracted from the infected patients
in the finger pads
 Recurrent herpes: Seen over keratinised
surfaces like palate and gingiva

65. Diagnosis & management of HSV
 Diagnosis:
• Immunoslot testing detects circulating viral antibodies
• Viral cultures and tissue biopsy are other alternatives
 Treatment:
• Self limiting disease which remains for 7-10 days
• Topical 5% Acyclovir cream is helpful reduce symptoms
• In extensive cases, oral Acyclovir 200mg five times for 10
days. Valacyclovir has more bioavailability
Differential diagnosis
1.Erythema mutiforme
2.Erosive lichen planus
3. Apthous ulcer
4. Pempigus vulgaris

66. Herpes Zoster virus infection
 Primary infection with varicella zoster virus
leads to varicella (chicken pox).
 Reactivation of latent virus in the dorsal root ganglia
of cranial nerves lead to herpes
zoster infection/shingles.
 Incidence: 1.5-3 cases per 1000 cases
 More common in older individuals (>75 years)
 Transmission usually by respiratory route.
 Incubation period: 1-2 weeks
 Postherpetic neuralgia is an uncommon sequelae
seen in older individuals.

67. Pathogenesis of Shingles and
Postherpetic Neuralgia

68. Clinical manifestations
 Primary VZV infection mostly occurs in first two
decades of life as maculopapular rash.
 HZI of skin occurs in adults and start with prodromal
symptoms like deep, burning skin sensation.
 Within 2-4 days vesicles are seen in a dermatomal
pattern unilaterally
 Oral & maxillofacial manifestations:
• Most commonly affects the ophthalmic div. of
trigeminal nerve
• Prodromal phase is characterised by burning mucosal
pain
• This is followed by appearance of clusters of 1-
5mm ulcers which heal within 14days

69. Diagnosis & Management of
HZV infections
 Oral swab for viral isolation using cell culture is best way for confirming
diagnosis. Real time PCR can also be used
 Treatment:
 Acyclovir (800mg five times a day)
 Valacyclovir (1000mg three times a days)
 Regimen shoud be started within 72hrs of onset
 Postherpetic neuralgia:
• First line of treatment is 5% lidocaine patch and topical capsaicin
• Second line of treatment is with pregabalin, opioid analgesics and TCAs
• Case reports suggest use of botulinum toxin in PHN
 Vaccination of older adults reduces incidence of HZ infections.

70. Ramsay-Hunt syndrome
 Uncommon complication of Herpes zoster
infection
 Involves the geniculate ganglion
 Clinical features:
 Bell’s palsy, vesicles of external ear and loss
of taste sensation in the anterior two thirds
of tongue
 Herpes zoster infections are more common
in immunocompromised individuals

71. Erythema multiforme (EM)
 Acute, self-limited, inflammatory mucocutaneous
disease.
 Commonly manifests in skin, oral mucosa
& genitalia
 Represents hypersensitivity reactions to
medications or infectious agents(e.g: Pneumonia,
HSV, mycoplasma)
 Two types: (Acc. To Burket)
1) Erythema multiforme minor- < 10% of
total body skin
1) Erythema multiforme major- More extensive skin &
mucosal involvement

72. Clinical findings
 EM generally affects individuals between
20-40 years
 Prodromal phase is characterised with
fever, malaise and headache, cough,
rhinorrhea
 Target/ iris lesions are pathognomonic
of EM
 Oral cavity lesions shows painful
erythematous ulcerations, lips show
haemorrhagic crusting

73. Management of EM
 Mild oral EM can be managed with systemic/ topical analgesics for
pain and supportive care since the disease is self-limiting
 More severe cases are manged with topical/ systemic corticosteroids
 Acyclovir may be added if HSV infection is suspected
 However, Marx & Stern contraindicates the use of steroids in EM
minor as they are saying use of steroids increase the chance of
infections

74. Stevens-Johnson Syndrome
 Also known as Erythema multiforme major
 Life threatening and debilitating hypersensitivity
 Characterised by an intense vasculitis due to a combined type III
& IV hypersensitivity
 Age: Less than 15 years
 Clinical features: Triad of oral, ocular and genital lesions
 SJS has an explosive onset and progress very rapidly
 Treatment:
 Emergency condition, requires intense supportive care
 Fluid resuscitation is required to prevent dehydration
 Systemic corticosteroids(IV methylprednisolone 500mg) along
antibiotics coverage and immunosuppressive drugs
 Silver diazine creams are applied locally, protection of eyes

75. Necrotising ulcerative gingivitis
and periodontitis
 Represents an acute ulcerative-
inflammatory condition of the
gingiva and periodontium
 Associated with polymicrobial
infections
 Strong association with immune
suppression, diabetes, debilitation,
smoking, stress, poor oral hygiene,
local trauma, etc.
 Etiology: Fusospirochaetal
microorganisms
 In presence of systemic illness NUG
and NUP can progress into cancrum
oris/ noma

76. Seven stages of ANUG -
Horning & Cohen
Stages
Stage I Necrosis of tip of papilla
Stage II Necrosis of entire papilla
Stage III Necrosis extending to marginal gingiva
Stage IV Necrosis extending to attached gingiva
Stage V Necrosis extending to labial & buccal mucosa
Stage VI Necrosis exposing alveolar bone
Stage VII Necrosis perforating skin of cheek

77. Clinical features
 Necrotising ulcerative gingivitis have a rapid
onset.
 First symptoms are excessive salivation, metallic
taste, sensitivity of gingiva.
 Disease rapidly progress into extremely painful
punched-out ulcers which starts from
interdental papilla.
 Differential diagnosis:
1. Primary herpetic gingivostomatitis
2. Desquamative gingivitis
3. Mucous membrane pemphigoid
 Laboratory tests: Gingival sulcular secretion
culture.

78. Treatment
 Management is directed toward supportive care, pain control and
identification of predisposing factors.
 Definitive treatment consists of gentle debridement to remove
plaque and debris under LA.
 Hydrogen peroxide is used for killing anaerobic microbes along with
chlorhexidine mouth wash.
 Beta lactams and Metronidazole are antibiotics of choice
 Patients must be tested for HIV
 Once the acute phase is over we perform scaling and root planing for
residual plaque removal.
 Periodontal surgery is needed to correct the periodontal defects.

79. Aphthous Stomatitis
 Also known as canker sores
 Pathogenesis: Believed to be
due to an immune-based
leukoclastic vasculitis
Types Clinical findings
Minor Most common, <1cm, lasts for 7-14 days, no scarring is seen,
occurs over free oral mucosa
Major >1cm, lasts for weeks, heals with scarring
Herpetiform <1cm, >10 ulcers, dispersed widely over oral mucosa
Severe Same as minor, but ulcers present continuously

80. Treatment of aphthous ulcers
 Minor aphthous ulcers are self-limiting and requires only
reassurance of the patient.
 Major aphthous ulcers are treated with a combination of antibiotics
and systemic steroids.
 Marx & Stern proposes three antibiotic regimens (2-6 months):
1. Erythromycin 250mg orally 4 times daily
2. Doxycycline 100mg orally once daily
3. Tetranydril elixir/ Magic mouth wash (Tetracycline 250mg+ 12.5 mg
Diphenhydramine HCl per 5ml of Kaopectate
 If these regimens fail we generally opt for systemic corticosteroid
regimen with prednisone.

81. Behcet syndrome
 Triad of recurring oro-genital ulcers and eye
involvement
 Occurs in young adults, male predilection seen
 Diagnostic criteria:
a) Recurrent oral ulcers: Aphthous type ulcers
which occur atleast 3 times in I year period
b) Plus 2 of the following:
1. Eye lesions: Uveitis, retinal vasculitis and
hypopyon
2. Skin lesions: Papulopustular genital lesions
3. Positive pathergy test
 Treatment: Systemic corticosteroid regimen I
or III with prednisone

82. Pemphigus vulgaris (PV)
 Pemphigus vulgaris falls in a group of
autoimmune, potentially life-
threatening disease.
 Characterized by blisters and erosions
of skin and mucous membranes due to
intraepithelial acantholysis.
 Etiology: Caused due to binding of
IgG autoantibodies to desmoglein 3 &
1( transmembrane adhesion
molecules) present on desmosomes.
 Incidence: 0.1-0.5 cases per 1 lacs per
year

83. Clinical manifestations of PV
 Classic lesion of PV consists of a thin-walled bulla arising on an otherwise
normal skin/ mucosa.
 These bullae rupture and continue to extend peripherally leaving areas of
ulcerated mucosa and denuded skin ( Lutz sign).
 Nikolsky sign: Pressure application on an apparently normal area of skin
results in formation of a new lesion.
 Oral lesions precede the lesions of skin
 Diagnosis:
1. Direct immunofluorescence
2. Indirect immunofluorescence
3. Biopsies are best done on intact vesicles < 24hrs old

84. Differential diagnosis of PV
1. Herpes simplex virus infections: Affects young children,
acute onset
2. Erythema multiforme: Acute nature, patient gives history
of taking medications in most cases, target lesions are seen
3. Recurrent aphthous stomatitis: Aphthous ulcers are
round and symmetrical. They tend to heal and recur. But in
pemphigus, the same lesions continue to extend
peripherally in a chronic nature.
4. Mucous membrane pemphigoid: Distinguished by
indirect immunofluorescence

85. Treatment of Pemphigus vulgaris
 Most important aspect is early diagnosis of the disease when lower
doses of medication can be used for shorter periods of time to control
the disease.
 High doses of systemic corticosteroids (Prednisone) are given in
dosages of 1-2mg/kg/day
 Adjuvant therapy to reduce the side-effects of steroids include
azathioprine, mycophenolate, etc.
 Rituximab is presently used though there are reports of high infection
rates.

86. Mucous Membrane Pemphigoid
 Chronic autoimmune subepithelial disease which primarily
affects mucous membranes
 Age: More than 50 years
 Female:Male : 2:1
 Etiology: Primary lesion of MMP occurs when
autoantibodies directed against proteins in the basement
membrane zone cause a subepithelial split and vesicle
formation.
 Conjuctiva is the second most common site after oral cavity.
 Corneal damage, symblepheron and blindness are common
ocular manifestations.
 Desquamative gingivitis is the most common oral lesion

87. Treatment of mucous membrane
pemphigoid
 Patients with mild oral disease are
treated with topical and
intralesional steroids
 Ophthalmologists must be
consulted for the management of
ocular manifestation
 Systemic steroid therapy regimen
I & III are used in severe cases
Cicatricial pemphigoid
with symblepheron

88. Management of patients on
Corticosteroid therapy who require
Major surgery
 Patients who regularly take corticosteroids develop adrenal
insufficiency due to depression of HPA axis.
 According to Hupp, Ellis & Tucker:
1. If the pateint is currently taking steroids:
 Use anxiety-reduction protocol.
 Monitoring of vitals before, during and after surgery.
 Instruct patient to double usual daily dose on day before, day of,
and day after surgery.
 On second post op day advise the patient to return to usual
dose.

89. Management of patients on
Corticosteroid therapy who
require Major surgery
 According to Hupp, Ellis & Tucker:
2. If the patient is not currently taking steroids but has received
atleast 20mg of hydrocortisone or equivalent for >2 weeks in
past one year,
 Use anxiety-reduction protocol
 Monitoring of vitals before, during and after surgery.
 Instruct the patient to take 60mg hydrocortisone on the day
before and the morning of surgery
 On the first 2 post op days, the dose should be dropped to
40mg and dropped to 20mg for 3 days thereafter. The
clinician can cease administration of supplemental steroids 6
days after surgery.

90. References
 Burket’s Oral Medicine
 Oral & Maxillofacial Pathology – Marx & Stern
 Oral & Maxillofacial Surgery Clinics of North America (2006 issue)
 Van der Waal et al., Journal of Oral oncology (2000)
 Khanna, Andrade: Oral submucous fibrosis : A new concept of
management: Report of 100 cases; IJOMS 1995