1. The document discusses various types of oral lesions including vesicles, bullae, and ulcers. It classifies oral lesions based on etiology into categories like hereditary, traumatic, allergic, autoimmune deficiency, neoplastic, and miscellaneous. 2. Erythema multiforme is described as an immune-mediated disease that causes lesions on the skin and mucosa. It summarizes the characteristics, causes, clinical features, histopathology and management of erythema multiforme. 3. Pemphigus vulgaris is introduced as the most common form of pemphigus. It involves intra-epithelial blister formation and is characterized by separation of epithelial

1. GOOD MORNING

2. Guided By: PRESENTED BY:
Dr. S .R .Panat VERTIKA GUPTA
Dr. Prashant Gupta B.D.S(4th year)
Dr. Parag Agarwal 4th batch
Dr. Sonal Upadhyay

3. VESICLE : is an elevated blister containing clear fluid that
is under 1cm in diameter.
BULLAE: are elevated blister like lesions containing clear
fluid that are more than 1cm in diameter.
ULCER: is defined as a complete discontinuity of
epithelium caused by pathological processes in distinction
to the erosion which is a partial destruction of epithelial
structures with intact basal cell layers.

4. CLASSIFICATION-I
Hereditary Traumatic Allergic Auto Viral Neoplastic
Miscellaneous Immune
Deficiency
HEREDITARY: * Epidermolysis bullosa (EB).
TRAUMATIC: * Traumatic ulcer.
ALLERGIC: * Stomatitis medicamentosa.
* Stomatitis Venenata.
* Angioneurotic edema.
VIRAL : * Herpes simplex (IRHS).
* Herpangina.
* Hand-foot-and mouth (HFM) disease.
* Hoof and mouth disease (HM).

5. AUTO-IMMUNE DEFICIENCY:
* Erythema Multiforme EM.
* Acute epidermal neurolysis AEN.
* Stevens Johnson Syndrome.
* RAU-major-minor herpetiform.
* Behcet’s disease.
* Pemphigus vulgaris.
* Pemphigus vegetans.
* Bullous pemphigoid.
NEOPLASTIC:
* Oral Squamous cell carcinoma.
* Ulcers related to bone marrow depression.
MISCELLANEOUS:
* Cyclic neutropenia ulcers.
* Erosive Lichen planus.

6. CLASSIFICATION-II
NON-RECURRENT RECURRENT
* Single Traumatic * Single RAU
* Multiple – Acute * Multiple - Chronic
herpetic. ulcerative
stomatitis.

7. Erythema multiforme is an acute inflammatory disease of
the skin and mucous membrane that causes a variety of skin
lesions like macules, papules, vesicles, bullae which soon
ruptures into ulcers and erosions, giving it a ‘multiform’
appearance.

8.  EM MINOR - a milder self limiting form. It represents as a
localised eruption of skin with or no mucosal involvement.
 EM MAJOR - severe life- threatning form. It represents
severe skin and mucosal involvement.
 STEVENS-JOHNSON SYNDROME - There is generalised
vesicle and bullae formation involving skin, mouth, eyes and
genitalia.
 TOXIC EPIDERMAL NEUROLYSIS(TEN) - it is also called as
LYELL’s disease. It occurs secondary to drug reaction and
results in sloughing of skin and mucosa in large sheets.

10. 1. EM is an immune-mediated disease that may be initiated
by deposition of immune complexes in the superficial
microvasculature of skin and mucosa or cell-mediated
immunity.
2. Drugs like Allopurinol, oxycam NSAIDS, Sulphonamides
Benzediazepine, Trimethoprim, anticonvulsants such as
carbamazepine, phenobarbital, phenytoin, penicillin.
3. Microorganisms like mycoplasma pneumoniae and HSV.
4. Vaccination, radiation therapy and occasionally other
diseases like Crohn’s disease, ulcerative colitis, infectious
mononucleosis, sarcoidosis & histoplasmosis.

11. 1. AGE & SEX- most frequently seen in children and young
adults and is rare after the age of 50yrs. More common in
males than females.
2.SITES- commonly involved area are hands, feet, extensor
surfaces of elbow and knees .In oral cavity commonly
involved areas are lip followed by buccal mucosa ,palate
,tongue and face.
3. ONSET- It has got acute or explosive onset with
generalized symptoms such as fever and malaise .It may be
asymptomatic and in less than 24 hours ,extensive lesions
of oral mucosa may appear.
4.APPEARANCE- It is characterised by macule or
papule,0.5cm-2cm in diameter ,appearing in segmental
distribution. More typical lesions contains petechiae in the
centre of the lesion.

12. 5 .TARGET/IRIS LESION/BULL’S EYE -consist of central
bulla and pale clearing area ,surrounded by edema and
band of erythema.
6 .STEVENS-JOHNSON SYNDROME -There is generalised
vesicle and bullae formation involving skin, mouth, eyes
and genitalia.
7 .TOXIC EPIDERMAL NEUROLYSIS(TEN)- It occurs
secondary to drug reaction and results in sloughing of skin
and mucosa in large sheets.

14. 1. It occurs along with skin lesions in 45% of the cases.
2. SITES- lip commonly followed by buccal mucosa, palate,
tongue and face.
3. APPEARENCE- oral lesions start as bullae,on an
erythmatous base and break rapidly into irregular ulcers.
4. SYMPTOMS- patient cannot eat or swallow and drools
blood tinged saliva.
5. SIGNS- * The lesions are larger, irregular, deeper and
often bleed very freely.
* In full blown cases, lips are extensively involved and large
portions of the oral mucosa are denuded of epithelium.
* Sloughing of mucosa and diffuse redness with bright red
raw surface is seen.
6. Healing occurs in 2 weeks.

16. The cutaneous or mucosal lesions generally exhibit
intracellular edema of the spinous layer of epithelium and
edema of superficial connective tissue, which may produce
subepidermal vesicle.
There is zone of liquefaction degeneration in the upper
layer of the epithelium with intraepithelial vesicle
formation and thinning, with frequent absence of basement
membrane.
Dilatation of the superficial capillaries and lymphatics in
the upper most layer of the connective tissue is prominent
and mixed inflammatory infiltrate with numerous
eosinophil also seen.

18.  Primary herpetic gingivostomatitis.
 Pemphigus vulgaris.
 Mucous membrane pemphigoid.
 Erosive lichen planus.
 ANUG.
 Dermatitis herpetiformis.
 Herpes zoaster.
 Chickenpox.

19.  MILD CASES: soft liquid diet and topical anaesthetic
mouthwash like Promethazine, topical syrups or elixirs-
diphenhydramine.
MODERATE TO SEVERE CASES:
• Short course of systemic corticosteroids- 30mg/day
prednisolone or methyl prednisolone for several days and
tapered after the symptoms subsides.For severe cases,higher
doses of steroids are necessary.
• Prophylatic Acyclovir to prevent HSV related EM.
TEN CASES:
• i.v administration of pooled human immunoglobins.

20. Pemphigus is a auto-immune disease involving the skin &
mucosa and characterised by intra – epithelial bullae
formation.
VARIENTS OF PEMPHIGUS:
Pemphigus vulgaris.
Pemphigus vegetans.
Pemphigus foliaceous.
Pemphigus erythematosus.

21. It is most common form of pemphigus , accounts for 80% of
cases.
MECHANISM-
Binding of IgG antibody to pemphigus antigen leads to
epithelial cell separation by triggering complement activity
or plasminogen plasmin system.
Separation of cell takes place in lower layer of
S.spinosum.
It may be associated with thymoma , myasthenia gravis or
with multiple autoimmune disorders.
It may be triggered by drug therapy like pencillamine ,
pencillin , phenobarbital, captopril.

23. AGE & SEX- it is seen in 5th to 6th decade of life and male
to female ratio is 1:1, with whites more commonly effected.
SIZE- thin walled bullae or vesicles varying in diameter
from few mms to several cms arising on normal skin or
mucosa.
SIGNS- these lesions contain a thin, watery fluid but they
soon become purulent or sanguineous. They rapidly break
and continue to extend peripherally, leaving large areas of
denuded skin.
NIKOLSKY’S SIGN- after application of pressure to an
intact bulla, the bulla will enlarge by extension to
apparently normal surfaces and the pressure to apparently
normal area will result in formation of new lesion. It results
from upper layer of skin pulling away from the basal layer.

25. Basic defects are intra-epithelial & is demonstrated as
acantholysis in S.spinosum.
The cellular outlines are round, rather than polyhedral,
intercellular bridges are lost & nuclei are large &
hyperchromatic.
The underlying connective tissue is densely filled with
chronic inflammatory cells, which may also enter the
vesicular fluid.
As the vesicle & bullae rupture, the ulcerative lesion
becomes infiltrated with polymorphonuclear leucocytes
and the surface may show suppuration.

27. In 90% of cases oral lesions develop and in 60% cases
they occur first.
SITES- buccal mucosa is commonly involved, palate and
gingiva are other common sites.
ONSET -oral lesions begin as classic bullae or non-
inflammed base with formation of shallow ulcers as bullae
break rapidly.
SIGNS- thin layer of epithelium peels away in an irregular
pattern leaving denuded base.
NIKOLSKY’S PHENOMENON- the oral lesions may
exhibit Nikolsky’s phenomenon & may be denuded by
peripheral enlargement of the lesion.
SYMPTOMS- lesions bleed easily and are tender on
palpation.The pain may be so severe that the patient is
unable to eat.

29. MARGINS- the lesions may have ragged borders and be
covered with white or blood tinged exudate.
GINGIVA- diffuse erythematous involvement of gingiva.
DIFFERENTIAL DIAGNOSIS
 Recurrent apthous stomatitis.
 Dermatitis herpetiform.
 Viral infections.
 Bullous pemphigoid.
 Erythema multiforme.
 Bullous drug induced exanthema.

30. PV-ventral surface of tongue

31. BIOPSY -best for intact vesicles and bullae less than 24hrs
old, & is done from the advancing edge of the lesion to see
acantholysis.
TZANCK SMEAR -to demonstrate Tzanck cells which lie
freely within the vesicular space.
INDIRECT IMMUNO-FLUORECENT ANTIBODY TEST -
antibodies against intercellular substances can be seen. The
titers of antibody are directly related to the level of the
clinical disease.
DIRECT TEST -antibody will bind the immunoglobin
deposit in the intercellular substance & show positive
fluorescence.

33. CORTICOSTEROIDS - systemic prednisolone - 1 to 2 mg/
kg/day.
COMBINATION THERAPY- high dose of corticosteroids
+ immunosuppressive drugs such as Azathioprine,
cyclophosphamide, cyclosporine, mycophenolate.
PLASMAPHERESIS -useful in patient refractory to
corticosteroids.
OTHERS- parentral gold therapy, Dapsone , Etretinate,
Tetracycline.
NEWER THERAPY- administration of 8-methoxy-
psoralen(.6mg/kg), followed by exposure of peripheral
blood to UV radiation.

34. THANK YOU