Keratotic and non-

keratotic lesions of Oral

Cavity

Dr Sridevi

1
 Outine of lecture
• Classification of the non-keratotic lesions of oral cavity.
• Describe the etiopathogenesis and list the clinical
features of and their differential diagnoses.
• Relevant investigations to diagnose oral ulcers and red
lesions and formulate treatment plan.

References
1. Burket’s text book of oral medicine 11th edition
2. Hand book of oral diseases Crispan Scully

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 Introduction
• Many oral ulcerative or vesiculubullous lesion have similar erythematous
or red in clinical appearance either as,
• Macule
• Papule
• Ulcer
• Erosion
• Vesicle or Bullae
• Purpura

• Can be categorize by,

a. Length of time –acute or chronic
b. Past history of similar lesions- recurrence
c. Number of lesions present- single or multiple

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Red lesion -refers to an area of reddened mucosa that may
be smooth and "atrophic looking" or exhibits a granular,
velvety texture. Such lesions occur alone or with areas of
hyperkeratosis and are generally found only by more
careful examination than is required for demonstration of
most white lesions.

Atrophic epithelium.
Reduction in the no. of epithelial cells or increased
vascularization.

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 What is an - ULCER

• Defect or break in the continuity of the epithelial component of skin or

mucosa, so that a depression or punched out area exists with exposure
of the underlying connective tissue.

Ulcers are classified based on

– Duration and severity of symptoms

– Depending on the cause/source/etiology

Dr Sridevi 5
 Classification according to Etiology

1- Physical and chemical agents: 2-Microbial agents.

A-Bacterial:
(Reactive ulcers):
– Necrotizing ulcerative gingivitis.
• Traumatic.
– Tuberculosis.
• Thermal. – Syphilis.
• Chemical. B-Fungal:
• Electrical. – Histoplasmosis.
• Radiation. – Blastomycosis
C-Viral:
– Herpes simplex.
– Herpes Zoster.
– Herpangina
– Hand foot and mouth disease.

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3-Neoplasm 4- Immunologic reactions.
• Squamous cell carcinoma • Aphthous ulcers.
• Behcet’s syndrome
• Pemphigus vulgaris
5- Blood disorders:
• Mucous membrane pemphigoid.
– Anemia.
• Lupus erythematosus.
– Leukemia.
• Epidermolysis bullosa.
– Neutropenia
• Drug eruption

6- Drugs.
– Cytotoxic drugs.

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 Systemic diseases
i) Mucocutaneous disease

7- Gastrointestinal disease. – Behcet’s syndrome

– Lichen planus
• Coeliac disease.
• Ulcerative colitis. – Vesiculobullous diseases
• Crohn’s disease. ii) Haematological disorders

– Anaemia
– Leukemia

iii) Gastrointestinal disorders

– Coeliac disease (Gluten-sensitive

entropathy)
– Crohn’s disease

Dr Sridevi 8
 Important Causes of Oral ulcers

Mucosal Ulcers Vesiculo-Bullous Diseases

Infective
• Primary and recurrent Herpes
simplex.
• Herpes zoster and chickenpox
• Hand-foot-and - mouth disease
• Herpangina
Non-infective
• Pemphigus vulgaris
• Mucous membrane pemphigoid
• Erythema multiforme
• Contact allergy

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 Classification of ulcer based on mode of onset and
clinical presentation
1. Multiple ulcers
Acute multiple ulcers
1. Herpetic form ulcers- Herpes Simplex Infection
2. Erythema multiforme
3. Stevens Johnson Syndrome and Toxic Epidermolysis Necrolysis (TENS)
4. NUG & NUP
5. Oral ulcers secondary to cancer chemotherapy & or radiotherapy
6. Contact allergic stomatitis
7. Varicella zoster virus infection
8. Coxsackievirus infections
Chronic multiple ulcers
1. Pemphigus Vulgaris
2. Pemphigus vegetans
3. Paraneoplastic Vegetans
4. Bulluos Pemphigoid
5. Mucous Membrane Pemphigoid
6. Malignant ulcer

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2. Recurring ulcers
1. Bechet’s syndrome
2. Apthous ulcers
3. Herpetic ulcers
4. Cyclic neutropenia
5. Chronic idiopathic neutropenia

3.Single ulcers
1. Mucormycosis
2. Histoplasmosis
3. Traumatic ulcers
4. Eiosinophilic ulcer
5. Tuberculosis ulcer
6. Syphilitic ulcer
7. Neoplastic ulcer

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Acute multiple ulcers

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 Herpes simplex virus infection
• HSV1 – causes infection above the waist

• HSV 2- causes infection below the waist

Primary infection occurs at the site of initial contact , virus then travels along the nerve
exhibits latent infection.

Extra neuronal latency – virus remaining latent in the cells other than neurons
 Herpetic whitlow – fingers(dentists)
 Herpes gladiotorum – skin spread through sports of wrestling
 Herpes encephalitis, esophagitis
 HSV is recovered in endoneurial fluid of bell’s palsy patient

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 Clinical manifestations
Primary Gingivostomatitis
Has acute onset typically affects children below 6 years of age,
adults who are immunocompromised.
Prodromal systemic symptoms
fever, malaise, myalgia precede oral lesions by 2-3days.
Cervical lymphadenopathy occurs
Skin, mucous membrane, eyes CNS commonly affected.
Oral lesions
• multiple oral ulcers affecting all parts of the mouth,
• generalised gingival erythema with multiples vesicles or ulcers present which are 1
to 5mm in size which coalesce to form large ulcer with scalloped border and
marked surrounding erythema
• food intake is usually difficult.
• Condition is self limiting.
Diifferential diagnosis
Herpetiform aphthous ulcer
leukemia,
erythema multiforme and
stomatis medicamentosa. Dr Sridevi 14
Recrudescent oral HSV infection
 Asymptomatic
 Shed virus in saliva & oral secretion important risk for transmission following
Dental treatment
 Triggers for reactivation includes
Fever, UV rays, trauma, stress, menstruation, steroid therapy,
Immunocompromised patients

Recrudescent HSV on the lips –Recurrent herpes labialis or cold sores

Prodomal symptoms includes itching, tingling or burning sensation followed by
vesicles formation and ulceration and then cursting of lesion

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Laboratory investigation :
• Cell culture , PCR, Tzanck smear
• Immunoglobulin Titers : Primary Infection – (Ig)M titers, several weeks latter permanently
IgG titers (seroconversion)
Management :
Primary HSV children -
• Pain control: antipyretic, analgesic acetaminophen 3 times daily, anesthetic mouth washes like
dyclonine HCL 0.5%, 10ml used 4 times a day
• Suppotive care: Plenty of water (Hydration), Soft bland diet
• Acyclovir 200mg mg or 15 mg/kg 5 times a day for 10 days.
• Reduces fever & the risk of virus shedding & infectivity.
• Aspirin is contraindicated in children –Reye’s syndrome

Recurrent HSV – can be suppressed by reducing the triggering factors

RHL is self limiting, use of topical antiviral reduces shedding infectivity, size & duration of lesion
• Topical : 5% acyclovir ( Zovirax) cream qid /4d ,
• 3% penciclovir q2h/4d ,
• 10% docosanol cream 3-6times a day .
• Systemic: valacyclovir or famciclovir 500-1000mg for 3times/day.

• HSV in immunocompromised – Resistant to acycovir , foscarnet is the drug of choice .

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Varicella Zoster Virus (VZ) infection
• Primary infection varecilla ( chicken pox)

• Reactivation Herpes zoster infection (HZI) commonly called as shingles.

• Transmission – Respiratory route Incubation Period 2-3wks. Characterized by sudden onset of
generalised pruritic vesicular rashes affecting skin.
• Primary varecilla infection – first 2 decades of life , disease begins with low grade fever ,
malaise development of puritic maculopapular rash ----vesicle (dew drop like )------cloudy----
pustular----burst ---scab----crust falls in 1-2wks.
• Site – trunk ,face spread centrifugally.
• HZI increases with age, pts undergoing cancer chemotherapy, immunosuppressive drugs ,
AIDS.

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Shingles
 Adults , characterised by proderm of deep aching burning pain followed by eruption of
vesicules in zoosteriform pattern –
 unilateral, linear, clustered distribution of vesicles ,ulcers & scab in dermatome supplied by
one nerve – thorasic , lumbar frequently involved .
 Lesions heal in 2-4weeks with scarring, hypopigmentation.
 Immunocompromised pts experience HZI bilateral, involving multiple dermatomes.

Complication of HZI –
1. Post Herpetic Neuralgia
2. Ramsay Hunt syndrome ( uncommon )
3. Neuralgia induced osteonecrosis cavitation (Uncommon)

Post Herpetic Neuralgia (PHN )

• Pain that lingers 30-120days after the onset of acute rash
• Affects 50-80% of pts ->50yrs

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Site of occurrence – VZV infection
• Primary infection- minor acute ulcerations in mouth
• Recurrent –prodrome of pain, burning, tenderness with distinctive
unilateral distribution. Heal in 10-14 days.
• Involves V1 of Trigeminal nerve is most often affected, lesions on the
upper eyelid, forehead , scalp.
• V2 –painfull ulcers 1-5mm on hard palate, buccal gingiva. Ulcers collase to
form large ulcers with scalloped borders.
• V3- lesions in mandibular gingiva , tongue.

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Laboratory diagnosis
Cell culture , PCR, Smear, Immunoglobulin titers
Primary Infection – (Ig)M titres several weeks latter permanently IgG titres (seroconversion)
Management
Varicella & HZI is directed toward pain control, suppotive care & hydration.
Defenitive treatment to minimize the risk of transmission.
Systemic:
Acyclovir 800mg, 5 times/d – this reduces infectivity & severity of lesions
Valacyclovir 1000mg , 3 times/d or
Famciclovir 500mg 3 times /day for 7 days is effective in treating HZI should be started
within 72hrs to reduce the risk of PHN
 Live attenuated VZ vaccine for patients over 60yrs reduces the incidence of HZ &
sequele of PHN.

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Post Herpetic neuralgia

Management :
• First line of drug -gabapentine
• Topical Therapy – 5 % lidocaine patch or analgesic like capsaicin .
• Tricyclic Antidepressant such as amitriptylin , nortriptyline , doxepin can be used
to reduce chronic pain .
• Patients undergoing episodes of shooting pain may get relief through the use of
anticonvulsants such as CARBAMAZEPINE or PHENYTOIN SODIUM.
• Botulinum toxin
• When medical therapy is ineffective then nerve blocks or surgery at level of
peripheral nerve or dorsal root is effective.

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Coxsackievirus infection
Hand Foot Mouth disease – CVA 16 ,
• Occurs in children younger than 10yrs, summer infection
• Pts have low grade fever, sore mouth
• Skin lesions- hands & feet (dorsa, palms & soles)
• Oral lesions – hard & soft palate, tongue
Herpangina – CVA (1-10 ,16 ,22)
• Herpes- vesicular eruption, angina – inflammation.
• Sore throat pain on swallowing .
• There may be erythema of oropharynx ,soft palate, tonsillar pillars.
• D/D : streptococcal throat infections, HSV.
Laboratory tests:
Diagnosis usually made by clinical findings, culture nd biopies are rarely indicated.
Management:
• control of fever-antipyretics.
• oral pain - 2% viscous lidocaine (swiss & spit, liquid diphenhydramine 5ml 4-5 times
/day)
• supportive care – bland diet , frequent sipping of water (hydration)
• Limiting contact with others to prevent spread of infection.
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 ERYTEMA MULTIFORME
Mucocutaneous disease
• 20-40 yrs , recurrent EM have an average of 6 episodes /year.
• Skin lesion take several form hence multiforme.
• Classic lesion is target eye lesions.
Aetiology :
• Type III hypersensitivity reaction
• Most common trigger factors are
• Infections like HSV, Bacterial, fungal , protozoal infections &
• Drugs like Sulphonamides, barbiturates, NSAID’S, penicillins, cox-2 inhibitors,
phenothiazines are associated with EM.
• Skin lesions pathognomic lesion: target or iris or bulls eye lesion.
• 3 concentric zones: Target eye lesion
• a central intact bulla,
• edematous zone(pale pink) &
• outer erythematous zone(appears red)
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Oral lesions
• Lips & anterior part of oral cavity are frequently affected, manisfested as bullae, erosions or
ulcers which may or may not be covered by pseudomembrane . vermillion border of the lips
exhibits a Characteristic bloody crusted appearance.
• Lesions heal with scarring
• Attacks recur at the intervals of several months.
• Usually self limiting resolves in 3 to 5 weeks.

Management
• Mild EM managed with systemic & topical analgesics for pain & supportive care since disease is
self limiting & resolves within a few weeks.
• Cases suspected of HSV infection, Acyclovir 400mg twice a day prevents development of EM.
• Cases not related to HSV respond well to Azathioprine ( 100-150mg)
• In severe cases antibiotics are used to prevent any secondary infections.
• Dapsone 100-150mg/d
• Antimalarials like hydroxychloroquine are partially successful in suppressing recurrent
outbreaks.

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 Steven Johnson syndrome (SJS) (TENS)

• SJS is less severe variant of TENS & separate clinically

etiopathologically from EM.

• SJS Is associated with Drugs & Mycoplasma pneumoniae.

Management
– High doses of systemic corticosteroids,

– i.v immunoglobulin &

– thalidomide.

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Recurring ulcers

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 APTHOUS ULCERS
Etiology
1. Genetics factors
2. Hematological – deficiency serum iron, vitb12
3. Immunological abnormalities
4. Microbial agents- Helicobacter pyroli, HHV6, HH7,VZV.
5. Periods of pscychological stress, anxiety, local trauma, menstruation, food
allergy
6. Drugs, blood dyscrasias etc
Clinical features:
• May experience burning sensation for 2 to 48 hrs before ulcer appears.
• Localized area of erythema within hours
• Small white papule forms
• Ulcerate and increase over next 48 to 72 hrs
• Ulcers are regular and well defined surrounded by erythematous halo rim and covered by
yellowish-gray fibrinous pseduomembrane
3 Types
• Minor
• Major
• Herpetiform Dr Sridevi 27
Minor apthous ( mikulicz ulcer)
Tiny round to ovoid in shape,
involve non keratinized oral mucosa,
1 to 6 ulcers at any given point of time
measuring 2-4mm in diameter and heal without scarring.

Apthous major( Sutton’s ulcer;Periadenitis mucosa necrotica recurrans)

Ulcers are large up to 1cm,
involve even keratinized oral mucosa,
occur few in number 12 to 6 at a time, present for long duration &
heal in about 2 to 6 weeks with scarring.

Herpetiform ulcers
Present as crops of tiny pin head sized ulcers which coalesce together.
involve keratinized oral mucosa,
ulcers begin as tiny vesicles that subsequently ulcerate,
extremely painful tend to heal in about 10days &
almost immediately recur.

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Differential diagnosis
• Herpes simplex
• Hand-foot-and mouth disease
• Lupus Erythematoses
• Pemphigus vulgaris
• Cyclic neutropenia
How to differentiate from intra-oral herpes ulcers?

Recurrent Apthous Stomatitis (RAS) Recurrent Intraoral Herpes (RIHS)

Non-specific etiology Viral etiology
Wide range of age group Middle age
Freely movable mucosa involved Attached mucosa
Single or 2-3 ulcers at a time Multiple pinpoint ulcers
Non-specific finding on histopathology Tzanck cells on smear
No antibody titers Convalescent sera show viral
antibodies
Corticosteriods used Corsticosteroids contraindicated
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Treatment
 Primary goal is to
relief of pain,
reduction in duration of ulcer and
restoration of normal oral function
 Secondary goal is to
reduction in the frequency and severity of recurrence
maintenance of remission
Topical medications such as,
• Antimicrobial mouth washes- A doxycycline capsule of 100 mg in 10 mL of water
administered as a mouth rinse for 3 minutes or tetracycline 500 mg plus nicotinamide
500 mg administered 4 times daily may provide relief and reduce ulcer duration.

• Topical corticosteroids (TCs)

• Fluocinonide , clobetasole or Triamcinolone 0.1 percent (Kenalog in Orabase)
can be applied to ulcers two to four times a day
• Betamethasone sodium phosphate as a 0.5-mg tablet dissolved in 15 mL of water
to make a mouth rinse, used 4 times daily for 4 minutes each time.
• Dexamethasone elixir, 0.5 mg per 5 mL, may be used as a rinse and expectorated.
(Larger lesions can be treated by placing a gauze sponge containing topical steroid leaving it in
place for 15-30min to allow for longer contact of medication.) Dr Sridevi 30
 • Lidocaine 2% gel or spray for 3times a day for 1 week
• Amlexanox paste-3times a day for 1 week

 Intralesional steroid can be used to treat large indolent ulcers.

 Systemic medication when topical therapy is ineffective.
• Systemic steriods-prednisolone 20 mg, 40mg for 7-15 days
• Levamisole 150mg for 3 consecutive days then repeat after 2 weeks for 3
months.
• Colchicine- 1 to 1.5 mg/d
• Pentoxifylline 400 mg 3 times a day
• Dapsone 25 or 50 or 75mg/day for 3 days ,
• Thalidomide 100 mg/day can be considered.

(Teratogenicity and other potentially severe side-effects, thalidomide must be used with
caution in woman with child bearing age owing to potential for life threatening
deformities. )

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 Behcet’s syndrome
Betchet’s syndrome, described as triad of
recurring aphthous ulcers,
genital ulcers and
uveitis leading to blindness.
Age – 25 to 40 yrs.

• Patients suffer one of four patterns of disease:

• Mucocutaneous (oral and genital ulceration)
• Arthritic (joint involvement with or without mucocutaneous involvement)
• Neurological (with or without other features)
• Ocular (with or without other features).

 The oral aphthae of Behcet's disease are not distinguishable from common aphthae. They are
the most consistently found feature and frequently the first manifestation.

Dr Sridevi 32
* Diagnostic criteria *
• Recurrent oral ulceration occurring at least 3 times in a year
• Presence of at least two of the following
• Major criteria
• Recurrent genital ulcers
• Recurrent Eye lesions ( uveitis, retinal vasculitis & cells in the vitreous)
• Skin lesions erythema nodosum/papulo-pustular lesions/aceniform nodules
• Positive Pathergy test/ "Skin Prick Test"
• Minor criteria:
• Arthralgia or arthritis
• Gastrointestinal lesions
• Vascular lesions (mainly thrombotic)
• Central nervous system involvement

 Pathergy Test:
• The test is positive if there is an exaggerated response to a sterile needle puncture
of the skin, where such puncture is followed by pustule formation.

Dr Sridevi 33
Treatment:
No specific treatment, but oral lesions can be controlled by:
• Topical or intralesional corticosteroids (similar like apthous ulcer)

• Topical anaesthesia to alleviate pain (similar like apthous ulcer)

• Systemic corticosteroids in resistant cases (40-60 mg prednisone/day).

• Azathioprine and other immunosuppressive drugs combined with prednisone have shown to
reduce ocular as well as oral & genital involvement.

• Pentoxifylline , dapson, colchine & thalidomide used to treat mucosal lesions.

• Infliximab, ethanercept are active against mucocutaneous blood disorders.

Dr Sridevi 34
Chronic Ulcers

Dr Sridevi 35
 Pemphigus
• Group of autoimmune, potentially life threatening VB lesion that causes
blisters & erosions on skin mucous membrane.
• Desmoglein 1 & 3 is a glycoprotein that strengths the intercellular
connection.
• Immune reaction against these glycoprotein causes loss of cell to
adhesion resulting seperation of cells & formation of intraepithelial bullae.
• Susceptibilty to develop autoantibodies is genetically determined.
Variants of pemphigus are
1. Pemphius vulgaris
2. Pemphius Vegetans
3. Pemphigus Foliaceus & Erthematosus
4. Paraneoplastic pemphigus.

Dr Sridevi 36
 Pemphius Vulgaris
Age – 5th and 6th decades
Etiopathogenesis:
Binding of Ig autoantibodies- Desmoglein 1 and 3 to epithelial membrane
Features :
• Classic sign is development of bullae on non inflamed skin or mucosa, oral
lesions starts bullae on non inflamed base which rapidly rupture, enlarges
by peripheral extensions leaving behind large denuaded areas with tissue
tags.
• Nickolsky’s sign is positive.
• Common site: Buccal mucosa most common site followed by gingiva palate.

Differential Diagnosis
1. RAS
2. Lupus erythematosus
3. Erosive lichen planus
4. Viral ulcers
5. Erythema multiforme
6. Pemphigoid lesions
Dr Sridevi 37
Dr Sridevi 38
Investigations
1. Cytology- Tzanck cells
2. Biopsy – suprabasal intraepidermal bullae
3. Immunoflouresence tests: direct / indirect- deposition of
autoantibodies- fishnet appearance

Treatment
 Prednisolone- 0.5-1mg/kg/day or about 40-80 mg/per day is administered.
 Immunosuppressants like cyclophosphamide 50mg/day & the dose escalated to 100mg/day.
 Mouth washes like bezydamine HCL 0.15%
 Antiseptic chlorhexidine gluconate 0.2% can be used.
 Systemic steroid therapy consisting prednisone in divided doses daily can be used until the control of
lesion is achieved after which medication is withdrawn until new lesion develop.-Pulse therapy
 Recalcitrant cases treated with i.v plasmapheresis involves removal of 1 to 2 L of plasma per
procedure, procedure is being replaced by Intravenous Ig, which can reduce circulating levels
of pemphigus antibodies almost as rapidly and may be safer.

Dr Sridevi 39
 Mucous membrane Pemphigoid
(Cicatricial Pemphigoid)
• Age - > 50yrs
• Gender- > F
• Demonstrate IgG antigens against BP 180 (COLLAGEN TYPE XVII).
• Lesions occurs frequently on oral mucosa, gingiva followed by conjuctiva, laryngeal
mucosa .
• Lesions heals with scar formation.
• Scarring & adhesions develop between bulbar & papebral conjuctiva known as
symblepharon.

Dr Sridevi 40
Investigations
– Direct ImmunoFluorence IgG & complement are identified at the epidermal
side
– Indirect ImmunoFluorence using salt split technique antibody directed
towards the antibasement membrane zone.

Treatment
1. Mild or localised lesions treated with topical steroids & intralesional steroids.
2. Desquamative gingivitis treated with topical steroids in soft splints
3. Systemic steroid therapy consisting prednisone in divided doses daily can be
used until the control of lesion is achieved after which medication is
withdrawn until new lesion develop.-Pulse therapy
4. Recalcitrant cases treated with i.v plasmapheresis involves removal of 1 to 2 L
of plasma per procedure, procedure is being replaced by Intravenous
immunoglobulin(Ig), which can reduce circulating levels of pemphigus
antibodies almost as rapidly and may be safer.
5. When topical & intralesional therapy is not successful; Tetracycline, doxycyclin
or minocycline is helpful.
6. When there are severe oral & conjunctiva, laryngeal involvement dapsone
therapy is recommended. Dr Sridevi 41
Single ulcers

Dr Sridevi 42
 Traumatic injuries causing single ulcers
Types of trauma
 Mechanical:
• sharp tooth,
• ill-fitting prostheis,
• orthodontic brackets,
• tooth brush etc)

 Chemical:
• Aspirin- aspirin burn.,
• concentrated clove oil,
• sodium hypochlorite,
• hydrogen peroxide,
• root canal medicaments etc
 Thermal :extremely hot or cold insults such as hot cheese, hot beverages etc- pizza
burns
 Self- inflicted – eosinophilic ulcer
• Lesions seen on the ventral surface of the tongue in infants rasping against newly erupted
primary incisors condition known as Riga-Fede disease.
• Self inflicted injuries in pts with familial dysautonomia often develop such ulcerative lesions .

 Iatrogenic :injuries caused by high speed rotary instruments, cotton

Dr rolls etc.
Sridevi 43
Differential Diagnosis
– Apthous ulcer
– Tuberculos ulcer
– Fungal infection etc

Management:
– Consumption of soft and bland diet
– Removal of traumatic factor
– Dentists should be aware of taking protective measures when using caustic substances &
heated instruments.
– Advised to rinse with warm saline
– Topical application of antiseptic and / anesthetic medication and mouth washes like
• Choline salicylate,
• Lignocaine
• Benzydamine hydrochloride etc
– Topical application of corticosteroid- Triamcinolone acetonide 0.1% if not relived with
anesthetic agents.
– Deep seated ulcers antibiotics- amox 500mg to prevent secondary infections.
– Self inflicted ulcers refer to psychiatrist for behavior modification therapy.
Dr Sridevi 44
Syndromes associated with oral ulcers

1. PFAPA Syndrome (Periodic Fever, apthae, pharyngitis,adenopathy)

2. MAGIC Syndrome( mouth apthae, genital lesions & interstitial

chondritris)

3. Behchet’s syndrome

4. Reiter’s syndrome

5. Steven -Johnson syndrome

6. James –Ramsay- Hunt syndrome

Dr Sridevi 45
 Red Lesion of oral cavity
• Is defined as area of reddened mucosa that may be smooth and atrophic looking or
exhibit granular, velvety texture.
• Can be congenital red lesions:
• Vascular malformation liken hemangioma, AV shunts etc

• Acquired red lesions:

1. Erythroplakia
2. Lupus erythemotosus
3. Stomatitis secondary to nutritional deficiencies
4. Radiation induced mucositis
5. Contact stomatitis
6. Arophy or erosion of mucosa like Erythemotous candidiasis, Atrophic lichen
planus
7. Inflammation secondary to Thermal burns, chemical burns, vascular dilation etc

Why Red?
 Atrophic epithelium
 Reduction in the number of epithelial cells.
 Increased vascularisation
 Extravasation of blood Dr Sridevi 46
 ERYTHROPLAKIA
Erythroplakia
• Erythroplakia is defined as “a red patch that cannot be clinically or
pathologically diagnosed as any other condition.” (11th edition Burket’s).

Shear described
a) Homogeneous erythroplakia.
b) Erythroplakia interspersed with patches of leukoplakia.
c) Granular or speckled erythroplakia.

Relative Frequency/incidence/prevalence:
• It is generally accepted that OE is much less common than Oral Leukoplakia (OL)
• In a survey of 50,915 Indian individuals, Mehta et al.(1975) found only nine
cases of Oral Erythroplakia (0.02%-0.1%)
• Site- Ventral tongue, floor of the mouth , soft palate and anterior tonsillar pillar

Dr Sridevi 47
 Differential Diagnosis
Clinically similar lesions may include
• Erythematous OLP.
• erythematous candidiasis,
• areas of mechanical irritation,
• denture stomatitis,
• vascular lesions,
• Nonspecific inflammatory lesions.

• Diagnosis is confirmed by biopsy

• 80 to 90% of cases of erythroplakia are histopathologically severe
epithelial dysplasia, carcinoma in situ, or invasive carcinoma.
• Treatment – In cases not showing carcinoma in situ , medical
management similar to leukoplakia , but ones showing dysplastic changes
– surgical management.
• Prognosis
– Fair to good depending upon microscopic diagnosis
– Almost all cases are premalignant to malignant upon initial discovery
Dr Sridevi 48
 Stomatitis secondary to nutritional
deficiency/ Anemic Stomatitis

• Pernicious anemia, iron deficiency anemia usually affect the oral

mucosa.

• Clinical features: The oral manifestations are early and common, and
are characterized by an atrophic, smooth and red tongue. A burning
sensation, taste loss, angular cheilitis may be present.

• Differential diagnosis
– Atrophic lichen planus
– Erythmoatous candidiasis
– Allergic stomatitis.

• The diagnosis is based on hematological laboratory tests.

• Management: treat the cause by supplements or good nutrition

Dr Sridevi 49
Radiation induced Mucositis
• Mucositis is an acute injury to the mucosal lining of the head and neck (HN)
region associated with cancer treatment.
• The clinical recognition of mucosal changes range from mild erythema to deep
mucosal ulceration.
• RIM may take weeks to months to heal depending on mucosal stem cell recovery.
• Palliation of symptoms of mucositis may be achieved by use of bland oral rinses,
topical anaesthetics.
Coating agents saline , bicarbonate, milk of magnesia, sucralfate, kaopectate &
water have been suggested for hydrating & diluting by rinsing.

Dr Sridevi 50
 Benzydamine hydrochloride is found to be effective in reducing the signs &
symptoms of mucositis
 Oral capsiacin is found to be effective in reducing the oral pain.

Use of radioprotective agents such as : amifostine before radiotherapy

Stimulation of salivary secretion

 Pilocarpine 5-10mg tid – risk of CV effects.

 Bethanocol 75-200mg/d in divided

 Mouth wetting agent may be used when it is not possible to stimulate salivary secretion.
Artificial salivary substitues like carboxymethlycellulose.

 Frequent sipping of water & moist diet are mandatory.

Dr Sridevi 51
Erythematous candidiasis
Denture induced stomatitisis

Diffuse erythematous area

 It was previously referred as atrophic oral candidiasis.
 Antibiotic sore mouth, a common form of atrophic candidiasis.
 Patients with chronic iron deficiency anemia may also develop atrophic
candidiasis.
 Erythematous candidiasis may be considered a successor to
pseudomembranous candidiasis but may also emerge de novo.
 Palate and dorsum of the tongue most commonly affected.
 Predisposing factors:- smoking
- broad-spectrum antibiotics.
 The lesion has a diffuse border where as erythroplakia has sharp
border.

Dr Sridevi 52
 Contact stomatitis/ Stomatitis Venenata
• Stomatitis medicamentosa- used fro effects of systemically administered drugs
• Stomatitis venenata (Contact Stomatitis) used for effects induced by topical
application of drugs or due to contact.

Etiology based on immune mediated or non-immune mediated hypersensitivity reaction.

Types of Contact Stomatitis:

i. Allergic contact stomatitis
ii. Irritant contact stomatitis

Agents causing stomatitis are

Dentifries
Mouthwashes
Dental materials
Food coloring and flavouring agents
Preservative etc…
Management:
Avoiding contact with the suspected irritant or allergen
Tooth paste and mouthwashes with strong flavouring agents must be avoided.
Topical: traimcinolone acetonide or flucinonide 0.05% can be used.
Dr Sridevi 53
Differential Diagnosis :
1. Erosive lichen planus
2. Stomatitis due to Anemias, vitamin B complex
deficiency
3. Allergic stomatitis

Treatment:
Topical antifungal – 7-14days
• Clotrimazole 2 % gel for 2 weeks
• Nystatin 5 lakh units tablets 4 times /day for 2 weeks- swiss
and swallow
• Fluconozole- dispersible tablet 3 times per day for 2 weeks-
mouth rinse.
Systemic
• Fluconozole 150mg 2 times for 14 days
• Ketconozole 200mg once for 1-4 weeks.

Dr Sridevi 54
 BENIGN MIGRATORY GLOSSITIS geographic tongue)
(erythema migrans, wandering wash, erythema areata migrans, stomatitis areata
migrans)
• Geographic tongue is an annular lesion affecting the dorsum and margin of the
tongue.
• The typical clinical presentation comprises a white, yellow, or gray slightly
elevated peripheral zone.
• Spontaneous development and regeneration of affected areas accounts for the
terms like- wandering wash, migratory glossitis and geographic tongue.
• Tongue lesions are occasionally associated with similar-appearing ectopic lesions
on the palate, buccal mucosa, or gingiva called erythema circinata migrans or
ectopic geographic tongue or annulus migrans.
• Prevalence: 1--2.5%
• Male=female
• Geographic tongue is circumferentially migrating and leaves an erythematous
area behind, reflecting atrophy of the filiform papillae.
• Symptoms: burning, stinging and pain of the tongue.
55

Dr Sridevi
Geographic tongue has also been seen with increased frequency in
patients with:
-pernicious anemia.
-pregnant patients-folic acid deficiency or
hormonal fluctuations.
-Psoriasis.
-Stress
-Asthma, Eczema, and Hay fever.
-Juvenile diabetes.
-Reiter’s syndrome- (arthritis, uveitis or conjunctivitis and
urethritis).

• A geographic appearance can be seen at other sites of the oral mucosa

than on the dorsum of the tongue- GEOGRAPHIC STOMATITIS.
• Fissured tongue should be interpreted as an end stage of geographic
tongue.

Dr Sridevi 56
Thank you

Dr Sridevi 57