This document defines and describes various oral lesions including vesicles, bullae, erosions and ulcers. It then discusses the potential causes of acute multiple lesions, recurring oral ulcers, chronic multiple lesions and single ulcers. Specific conditions that may present as oral ulcers are also outlined such as pemphigus vulgaris, mucous membrane pemphigoid, deep mycoses involving histoplasmosis, blastomycosis and mucormycosis.

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WARM GREETINGS

3.  VESICLE:
Elevated blisters containing clear fluid
that are less than 1 cm in diameter.
 BULLAE:
Elevated blisters containing clear fluid
that are greater than 1 cm in diameter.

4.  EROSIONS:
Red lesions often caused by the rupture
of vesicles or bullae or trauma and are
generally moist on the skin.
 ULCERS:
Well circumscribed, often depressed
lesions with an epithelial defect that is
covered by a fibrin clot, causing a yellow
white appearance. Ex. apthous ulcer.

5.  THE PATIENT WITH ACUTE MULTIPLE LESIONS:
-Herpes simplex virus infections
-Varicella zoster virus infections
-Cytomegalovirus infections
-Coxsackievirus infections
-Necrotizing ulcerative gingivitis &
periodontitis
-Erythema multiforme
-Stevens Johnson syndrome & toxic epidermal
necrolysis (Lyell disease)
-Oral hypersensitivity reactions.

6.  THE PATIENT WITH RECURRING ORAL ULCERS:
-Recurrent apthous stomatitis
-Behcet syndrome
 THE PATIENT WITH CHRONIC MULTIPLE
LESIONS:
-Pemphigus vulgaris
-Paraneoplastic pemphigus
-Pemphigus vegetans
-Subepithelial bullous dermatoses
.Bullous pemphigoid
.Mucous membrane pemphigoid
(cicatricial pemphigoid)

7. .Linear IgA disease
.Epidermal bullosa aquisita
.Chronic bullous dermatoses of childhood.
THE PATIENT WITH SINGLE ULCERS:
-Traumatic injuries causing solitary
ulcerations
-Traumatic ulcerative granuloma
(eosinophilic ulcer of tongue)
-Histoplasmosis
-Blastomycosis
-Mucormycosis(Phycomycosis)

8.  Most common form-80%
 Binding of IgG autoantibodies to DSG3,a
transmembrane glycoprotein adhesion
molecule present on desmosomes.

9.  This glycoprotein strengthens the
intercellular connection.
 Loss of this connection due to the antibody
antigen reaction weakens and finally breaks
the connection between epithelial
cells,resulting in blisters & desquamation.

10.  Patients with PV involving both skin &
mucosa have antibodies against Both DSG 1 &
DSG 3.
 Involving only mucosa with antibodies against
DSG 3.

11.  Thin walled bulla arising on normal skin or
mucosa.
 Bulla rapidly breaks but continues to extend
peripherally, eventually leaving large areas
denuded of skin.

12.  NIKOLSKY’S SIGN:
Results from the upper layer of the skin
pulling away from the basal layer.
 On application of pressure to an intact bulla,
it enlarges by extending to an apparently
normal surface.
 Pressure to an apparently normal area results
in the formation of a new lesion.

13. Thin walled
bullae between
fingers

15.  80-90%-develop during the course of the
disease.
 60%-oral lesions are the first sign.
 Extensive labial involvement-common.

16. The bulla is
intraepithelial
because of
acantholysis

20. Shallow
irregular
erosions

21.  Classic bulla on an non-inflammed base.
 Bulla rapidly breaks & clinician sees shallow
irregular ulcers.
 A thin layer of epithelium peels away in an
irregular pattern, leaving a denuded base.

22.  The edges of the lesion continue to extend
peripherally over a period of weeks until
they involve large portions of the oral
mucosa.
 Lesions start on the buccal mucosa, in areas
of trauma along occlusal plane.
 Palate & gingiva are other common sites.

23.  DIFFERENTIAL DIAGNOSIS:
1.Acute viral infections- acute nature
2.Erythema multiforme- acute nature
3.Recurrent apthous stomatitis- heal &
recur, acute nature, round & symmetric,
whereas PV is shallow & irregular, detached
epithelium at periphery.

24.  LABORATORY FINDINGS AND PATHOLOGY:
 Biopsies done on intact vesicle & bullae less
than 24 hours old.
 Pressure can be applied on the mucosa to
produce a new lesion and then biopsed.
 Advancing edge of the lesion which shows
characteristic suprabasilar acantholysis.

26.  Second biopsy from perilesional mucosa or skin
for DIF (Direct immunofluorescence)
 Placed in Michel’s transport medium.
 In the lab, fluorescein-labeled antihuman
immunoglobulins are placed over the patient’s
tissue specimen.
 Detect antibodies, usually IgG and complement,
bound to the surface of the keratinocytes.

28.  Indirect immunofluorescene:
distinguishes pemphigus from pemphigoid
and other chronic oral lesions.
 serum from a patient with bullous disease is
placed over a prepared slide of an epidermal
structure (usually monkey esophagus).

29.  The slide is then overlaid with fluorescein-
tagged antihuman gamma globulin.
 Patients with PV have antikeratinocyte
antibodies against intercellular substances
that show up under a fluorescent
microscope.

30.  Based on disease severity and progression.
 high doses of systemic corticosteroids,usually
given in dosages of 1 to 2 mg/kg/d.
 Prednisone-initially high dose to bring the
disease under control and decreased to lowest
maintenance dose.

31.  Adjuvants (immunosuppresants):
1.Mycophenolate mofetil
2.Azathioprine
3.Cyclophosphamide
4.Cyclosporine
 Dapsone
 Parenteral gold therapy
 i.v immunoglobulins
 Plasma exchange

32. Denuded
areas with
vegetations

33.  Autoimmune reaction that weakens a
structural component of the basement
membrane.

34.  subepithelial blistering diseases
 Binding of autoantibodies to specific antigens
(BP-180 & 230) found in the lamina lucida
region of BM,
causing localised damage, resulting in vesicle
formation in subepithelial region.

35.  Clinical manifestations:
 adults over the age of 60 years.
 Blister on an inflammed base, involves scalp,
arms, legs & groin.
 Pruritis of skin lesions.
 Bullae do not continue to extend
peripherally to form large denuded areas
unlike pemphigus.

37.  ORAL FINDINGS:
 Less severe, smaller & less painful than PV.
 No extensive labial involvement unlike PV.
 C.site:Gingiva
 Desquamative gingivitis with localized areas
of discrete vesicle formation.

38.  DD:
 Pemphigus
 Subepithelial bullous dermatoses
 Erosive lichenplanus

39.  LAB FINDINGS:
 Seperation of epithelium from CT.
 DIF: Deposition of IgG & C3 in BM.
 IIF: IgG antibodies bound to epidermal side
of salt split skin.
 Differentiates BP from EBA that has
antibodies localized to dermal side of salt-
split skin.

40.  Management:
High potency topical steroids- Clobetasol or
betamethasone.
With extentive disease, Systemic steroids and
other adjuvants are used.

41.  patients over the age of 50 years, resulting in
mucosal ulceration and subsequent scarring.
 Autoantibodies directed against proteins in
the basement membrane zone, causing
subepithelial split and subsequent vesicle
formation.

42.  IgG directed against antigens on the epidermal
side of the salt-split skin, which have been
identified as BP 180 (also called type XVII
collagen).

43.  C/F:
 Over 50 years
 Women
 Oral mucosa, Conjuctiva,Larynx,esophagus.
 Conjuctiva:
Scarring and adhesions developing between
the bulbar and palpebral conjunctiva called
symblepharon.

46.  Oral Manifestations in 90%:
 Desquamative gingivitis is the most common.
 Vesicles & erosions.

50.  DIAGNOSIS:
 Biopsy specimens taken from MMP patients
demonstrate positive fluorescence for
immunoglobulin and complement in the
basement membrane zone.

53.  MANAGEMENT:
 Systemic steroids-initially
 Topical steroids in soft splints for gingival
desquamation.
 Dapsone
 Tetracycline, doxycycline,minocycline.

55.  most common cause-trauma
 Trauma caused by
 teeth,
 food,
 dental appliances,
 dental treatment,
 heat,
 chemicals, or
 electricity.

56.  chronic oral ulcer
 DD
 deep mycoses histoplasmosis,
 blastomycosis,
 mucormycosis,
 aspergillosis,
 cryptococcosis, and
 coccidioidomycosis
 a chronic herpes simplex infection
 Syphilis
 scc

57. Traumatic ulcer of
the buccal mucosa
secondary to cheek
biting.

58.  Infection with a saprophytic fungus that
normally occurs in soil or as a mold on
decaying food.
 The organism represents an opportunistic
rather than a true pathogen

59.  In individuals with decreased host resistance,
such as those
 with poorly controlled diabetes
 hematologic malignancies,
 those undergoing cancer chemotherapy
 immunosuppressive drug therapy

60.  In the debilitated patient, mucormycosis may
appear as a
 pulmonary,
 gastrointestinal,
 disseminated, or rhinocerebral infection.

61.  inhalation of the fungus ,which invades
arteries and causes damage secondary to
thrombosis and ischemia.
 fungus may spread from the oral and nasal
region to the brain causing death

62.  Symptoms include
 nasal discharge caused by necrosis of the
nasal turbinates,
 ptosis,
 proptosis secondary to invasion of the orbit,
 fever,
 swelling of the cheek
 paresthesia of the face.

65.  ulceration of the palate, which results from
necrosis due to invasion of a palatal vessel
 gingiva, lip, and alveolar ridge
 large and deep, causing denudation of
underlying bone

66.  DIAGNOSIS
 Histopathologic specimen shows necrosis and
nonseptate hyphae ,which are best
demonstrated by a periodic acid–Schiff stain.
 Culture

67. Palatal Ulcer in
patient
taking
immunosuppressive
drugs

68.  TREATMENT
 surgical débridement of the infected area
 Systemic administration of amphotericin B
for up to 3 months

69.  caused by the fungus Histoplasma
capsulatum,
 inhaling dust contaminated with droppings,
particularly from infected birds or bats.
 manifesting as a self-limiting pulmonary
disease that heals to leave fibrosis and
calcification
 Disseminated to liver, spleen, adrenal glands,
and meninges

70.  Oral findings
 Appear as a papule, a nodule, an ulcer, or a
vegetation.
 Lymphadenopathy

71.  DIAGNOSIS
 culture of infected tissues or exudates on
Sabouraud’s dextrose agar
 Biopsy of infected tissue shows small oval
yeasts within macrophages and
reticuloendothelial cells & chronic
granulomas, epithelioid cells, giant cells, and
occasionally caseation necrosis.

72.  TREATMENT
 ketoconazole or itraconazole for 6 to 12
months.
 In severe cases, Intravenous amphotericin B
for up to 10 weeks

73.  caused by Blastomyces dermatitidis.
 Infection by inhalation from the soil.
 Associated with pulmonary symptoms.

74.  Oral manifestations
 nonspecific painless verrucous ulcer with
indurated borders

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