Ulcerative, Vesicular and

Bullous Lesions

Dr. sonia gulia

Pg second year
 CLASSIFICATION Burket’s 11 th edn.
• Herpesvirus Infections • Recurrent Aphthous
• Primary Herpes Simplex Virus Infections Stomatitis
• Coxsackievirus Infections • Behçet’s Syndrome
• Varicella-Zoster Virus Infection • Recurrent Herpes Simplex
• Erythema Multiforme Virus Infection
• Contact Allergic Stomatitis THE PATIENT WITH
RECURRING ORAL
• Oral Ulcers Secondary to Cancer Chemotherapy
ULCERS
• Acute Necrotizing Ulcerative Gingivitis

THE PATIENT WITH ACUTE

MULTIPLE LESIONS • Histoplasmosis
• Blastomycosis
• Pemphigus
• Mucormycosis
• Subepithelial Bullous Dermatoses
• Herpes Simplex Virus Infection in
Immunosuppressed Patients
THE PATIENT WITH
THE PATIENT WITH SINGLE ULCERS
CHRONIC MULTIPLE
LESIONS
Patient with (primary ) acute multiple
lesions
Herpes Simplex Virus (HSV) Infection
 Herpes Simplex Virus (HSV) Infection
• Etiology and
Pathogenesis
HSV-1, and α
herpes virus

• Initial contact with

Primary
infection
body secretion
• Mucosa, skin, eye

• Latent sites
recurrent
• oral & genital
mucosa, eye
Etiology
• Herpes simplex virus (HSV)
• Over 95% of oral primary herpes due to HSV-1
• Physical contact is mode of transmission
• 0.5 and 5 years of age.
• Incubation period of up to 2 weeks
• Abrupt onset in those with low or absent
antibody to HSV-1
Clinical Manifestations
• Primary gingivostomatitis
- Children and teenagers
- Viral prodrome of fever, loss of appetite,
malaise, and myalgia
- Erythema and clusters of vesicles and/or ulcers
- Keratinized mucosa -hard palate, attached
gingiva and dorsum of the tongue
- Nonkeratinized mucosa -buccal and labial
mucosa, ventral tongue, and soft palate.
• Recrudescent oral HSV infection
- Fever, ultraviolet radiation, trauma, stress, and
menstruation
- Recurrent herpes labiali
- Prodrome of itching, tingling, or burning
- Appearance of papules, vesicles, ulcers,
crusting, and then resolution of lesions
- Keratinized mucosa of the hard palate,
attached gingiva, and dorsum of the tongue
- 1 to 5 mm single or clustered painful ulcers
with a bright erythematous border.
• Immunocompromised patients
- Atypical- appearing ulcers
- Several centimeters in size
- Last several weeks or months
- Painful & may be larger
- Slightly depressed with raised borders
- Presence of 1 to 2 mm vesicles or satellite
ulcers at the edges of the main ulcer
 Diagnosis
• Cytology-Tzanck smear: multinucleated giant
cells, ballooning degeneration of nucleus
• Biopsy
• Serology: rising antibody titer
• Viral isolation-culture, PCR
• Immunpmorphological tests: direct
fluorescent assay, indirect
immunofluorescence
• Differential diagnosis
1. Coxsackievirus infections- ulcers not
clustered and the gingiva is not involved.
Viral culture or a cytology smear
2. Traumatic lesions
3. Apthous ulcers, fungal infection, and
neutropenic ulcers
 Treatment

• Soft diet and hydration

• Antipyretics (avoid aspirin)
• Chlorhexidine rinses
Management

Primary HSV Recurrent HSV Immunocomp

Infection • 5% acyclovir romised
• Acyclovir- 15 • 3% penciclovir • systemic
mg/kg five • 10% docosanol acyclovir
times a day and
• valacyclovir or
valacyclovir
famciclovir
Acyclovir , acyclor, (500– 1,000 mg
acyclar TID
Famcimac, penvir, virovir
 Varicella Zoster Virus (VZV) Infection
• Primary infection with VZV
• Latent, usually in the dorsal root ganglia or ganglia of
Varicella the cranial nerves
(chicken pox)

• Called shingles
• Elderly
Herpes zoster • Cancer chemotherapy, patients on chronic
infection (HZI) immunosuppressive drug therapy
• Clinical findings
- Low-grade fever, malaise, and the
development of an intensely pruritic,
maculopapular rash, followed by vesicles
• Vesicles- pustular, burst, and scab, with the
crusts falling off after 1 to 2 weeks.
• Dermatomal or “zosteriform” pattern
1st on trunk and face & spread centrifugally
• Heal - 2 to 4 weeks, with scarring and
hypopigmentation.
• Oral manifestations
Minor acute ulcerations in the mouth
Prodrome of pain, burning, and tenderness
Painful, clustered 1 to 5 mm ulcers
Unilateral distribution
Often coalesce to form larger ulcers with a
scalloped border
Heal within 10 to 14 days
Complication
Postherpetic Neuralgia
• Pain persisting for over a month after the
mucocutaneous lesions have healed
• > 60 years of age, < cell mediated immunity
• Pain, paresthesia, hyperesthesia, sensory
deficit
Diagnosis
• Clinical appearance and symptoms
• Cytologic smear with cytopathic effect present
(multinucleated giant cells)
• Viral culture or PCR examination of blister
fluid or scraping from base of erosion
• Serologic evaluation of VZV antibody
• Biopsy with direct fluorescent examination
using fluorescein labeled VZV antibody
 Differential Diagnosis
• Pulpitis- prodromal episodes of pain before
the onset of vesicles and ulcers
• HSV- appears in a similar fashion and if mild
and localized to one side may be mistaken for
HZI
• Acute necrotizing ulcerative periodontitis- in
severe cases of localized necrosis of the soft
tissues and bone
• Pemphigus vulgaris
• Mucous membrane (cicatricial) pemphigoid
Management
• Analgesic for pain control
• Acyclovir (800 mg five times a day)
• Valacyclovir (1,000 mg three times a day) or
famciclovir (500 mg three times a day) for 7
days
Postherpetic neuralgia
• Gabapentin and 5% lidocaine patch
• Opioid analgesics and tricyclic antidepressants
 Herpangina

Etiology
• Most often by members of coxsackievirus
group A (7, 9, 10,
and 16) or group B (1–5)
• Occasionally due to echovirus 9 or 17
Clinical Presentation
• Incubation period of 5 to 9 days
• Acute onset
• young children; summer
• Often subclinical
• Posterior oral cavity, tonsillar pillars involved
Macular erythematous areas precede short-lived
vesicular eruption, followed by superficial ulceration

• Accompanied by pharyngitis, dysphagia, fever, malaise,

headache, lymphadenitis, and vomiting
• Self-limiting course- under 2 weeks
Diagnosis
• Other viral illnesses to be ruled out or
separated
• Course, time of year, location of lesions,
contact with known infected individual
Differential Diagnosis
• Hand-foot-and-mouth disease
• Varicella
• Acute herpetic gingivostomatitis
Treatment
• Soft diet
• Hydration
• Antipyretics
• Chlorhexidine rinses
• Compounded mouth rinses
 Hand, foot and mouth disease
• Coxsackie A 16
• Fever, macules, papules, vesicles-hands and
feet
• Oral vesicles, ulcers
• CNS involvement, myocarditis, pulmonary
edema
• Treatment: supportive
Erythema Multiforme
(EM)
• acute, self-limited, inflammatory
mucocutaneous disease
• skin and often oral mucosa, & other mucosal
surfaces
• less than 10% of skin involvement
E M minor • no mucous membrane involvement

• more extensive
E M major • characteristic skin, oral mucosa and other
mucous membranes involved
• Etiology and pathogenesis
Inciting factors- infection
- Drug reactions
- food preservative
• Clinical Findings
between ages 20 and 40 years
Recurrent- 6 episodes a year
Prodrome of fever, malaise, headache, sore
throat, rhinorrhea, and cough
Skin lesions- “target” or “iris” lesion; itchy and
burnt
Postinflammatory hyperpigmentation
• Oral findings
Mild erythema and erosion to painful
ulcerations
Drooling of blood-tinged saliva
Lips (36%), buccal mucosa (31%), tongue (22%),
and labial mucosa (19%)
Irregular bullae, erosions, or ulcers surrounded
by extensive areas of inflammation
Differential diagnosis
• Primary HSV gingivostomatitis
• Pemphigus and pemphigoid
• Recurrent aphthous ulcers
 Management

Moderate to severe
HSV associated recurrent
oral EM
• 30 mg/d to 50 • acyclovir at 400 mg • dapsone,
mg/d of twice a day azathioprine,
prednisone/ levamisole
methylprednisolone • 400 mg of acyclovir
• azathioprine (100– bd or 500 mg of
150 mg/d) valacyclovir twice
Azimune, azoprine, azap, Acyclovir inj., acyclor, daily
zymurine acyclar Valcivir
Erythma multiforme Herpetic gingivostomatitis
Younger adults Small children
Exudative component in Apthous lesions over
the foreground general stomatitis
Target lesions No skin changes
Erythma multiforme Pemphigus

Young adult Older pts.

Acute Chronic

Erosive crusty changes Pustulopapular vegetation

Target lesions Skin changes in interiginous area

-ve nikolsky’s sign +ve nikolsky’s sign

 Stevens Johnson Syndrome (SJS) and
Toxic Epidermal Necrolysis (TENS)
• Medications, mycoplasma pneumoniae
• Severe lesions-erosions, bullae, ulcers, crusted
lips
• Chest> extremities-“atypical targets”
• Eyes, genitalia, mouth, skin
• Extensive oral ulceration with hemorrhagic
crusting of lip
• TEN more severe variant of SJS-sloughing of
skin & mucosa in large sheets, older people,
females
• Secondary infection, fluid & electrolyte
imbalance, involvement of lungs, liver, kidneys
 Necrotizing Ulcerative Gingivitis
(NUG) and Periodontitis (NUP)
• Acute ulcerative-inflammatory conditions of
the gingiva and periodontium
• Polymicrobial infection
• Immune suppression (especially AIDS),
debilitation, smoking, stress, poor oral
hygiene, local trauma, and contaminated food
supply, diabetes.
• Pathogenesis
Fusobacterium necrophorum

underlying Rapid destruction

Microbial infection
systemic illness of tissues

Production of cancrum oris,

endotoxins/ NUG and NUP noma, or orofacial
immunological
activation gangrene

Destruction of Reduced neutrophil

gingiva & adjacent chemotaxis and
tissue phagocytosis,
Clinical findings
• May or may not be associated with fever and
malaise
• Submandibular lymphadenopathy

Oral manifestations
• Excessive salivation
• Metallic taste
• Sensitivity of the gingiva
• Extremely painful and erythematous gingiva
• Scattered punched-out ulcerations
• Destruction of interdental papillae
• Malodor & gingival bleeding
NOMA
Differential diagnosis

• Primary herpetic gingivostomatitis

• Desquamative gingivitis such as mucous
membrane (cicatricial) pemphigoid,
pemphigus vulgaris, lichen planus, and
hypersensitivity reaction.
• Deep fungal infections
• Infections with the herpes family of viruses
• Squamous cell carcinoma
 Management
• Supportive care and pain control
• Removal of underlying predisposing factors
• Nutritional rehabilitation
• Gentle debridement of the lesional site under topical
anesthesia
• Chlorhexidine digluconate mouthrinse
• Antibiotic coverage (against gram-negative anaerobes)
• After resolution of acute phase; scaling and root
planning
• Periodontal surgery may be necessary to correct
gingival and periodontal defects
Recurrent Aphthous Stomatitis (RAS)
• Recurring ulcers confined to the oral mucosa
in patients with no other signs of disease
• Classified according to clinical characteristics:
Minor ulcers
Major ulcers (sutton disease, periadenitis
mucosa necrotica recurrens)
 Herpetiform ulcers
Etiology
• genetic factors
• hematologic deficiencies
• immunologic abnormalities
• local factors, such as trauma and smoking
• Anxiety, periods of psychological stress,
• menstruation
• upper respiratory infections
• food allergy
Clinical Presentation
• Recurrent, self-limiting, painful ulcers
• Usually restricted to nonkeratinized oral and
pharyngeal mucosa (not hard palate or
attached gingiva)
• Well-demarcated ulcers with yellow fibrinous
base and erythematous halo
• Minor variant (most common subtype)
• Single but more often multiple
• Healing without scarring in 10 to 14 days.
• Recurrent cases- 2 to 6 lesion in each episode

Major variant (Sutton’s ulcers)

• 1 cm or greater in diameter
• Single or less commonly several
• Deep to ragged edges with elevated edematous
margins
 Oral findings
• Frequently
prodromal during
burning before the
time second
from 2 to decade.
48 hours
• Round, symmetric, and shallow (similar to
viral ulcers), but no tissue tags are present
from ruptured
localized vesicles
area of erythema
• Multiple lesions
• Buccal smalland
whitelabial
papulemucosae
forms, ulcerates, and
gradually enlarges over the next 48 to 72
• Lesshourscommon on the heavily keratinized palate
or gingiva
Ulcers develops
Minor apthous
Major apthae
Herpetiform ulcers
 Differential Diagnosis
• Traumatic ulcer
• Chancre
• Viral stomatitis
• Pemphigus or pemphigoid
• Squamous cell carcinoma
• Chronic granulomatous disease
• Conditions associated with recurring ulcers, such
as connective tissue disease, drug reactions, and
dermatologic disorders
 Management
• Mild cases - protective emollient such as orabase
• Topical diclofenac
• Severe cases- high potency topical steroid
fluocinonide, betamethasone, or clobetasol
Floricot, clobetagen, clobetamil,

• Topical amlexanox paste and topical tetracycline-

mouthrinse or applied on gauze sponges
• Intralesional steroids- indolent lesions
• Non responsive cases- systemic therapy
colchicine, pentoxifylline, dapsone, short bursts
of systemic steroids, and thalidomide
Colchicindon, coljoy, thycad, thaloda
• Levamisole- 150 mg/ day for 3 consecutive
days--------gap of 2 wks-------repeat for 3 days.
• Done 6 times (3 mnths; 18 tabs.)
 Behçet Syndrome
• Triad - recurring oral ulcers, recurring genital
ulcers, and eye involvement.

Etiology
• Unknown
• Immune dysregulation
• HLA -B51 genotype is most frequently linked
Clinical Manifestations
Oral mucosa - most common site
• Genital area - ulcers of the scrotum, penis in
males and labia in females
• Eye lesions - uveitis, retinal vasculitis, vascular
occlusion, optic atrophy, and conjunctivitis
• Arthritis- knees, ankles, wrists, and elbows
- Joint may be red and swollen
- Permanent disability does not result
• Central nervous system involvement
• Other signs of BD include thrombophlebitis,
intestinal ulceration, venous thrombosis, and
renal, cardiac, and pulmonary disease

• Positive pathery sign is characteristic: sterile

pustule at site of sterile intradermal saline
injection 48 hours prior
Diagnosis
• Oral aphthous ulcerations occurring at least three times
per year in association with atleast 2 characteristic
manifestations within other systems (ocular, genital,
cutaneous problems +ve pathergy test)

Differential Diagnosis
• Erythema multiforme
• Reiter’s syndrome
• Crohn’s disease
• Mucous membrane (cicatricial) pemphigoid
• Vulvovaginal-gingival variant of erosive lichen planus
Treatment

• Systemic corticosteroids
• Immunosuppressive drugs (eg, interferon, TNFα
inhibitors)
• Azathioprine, cyclosporine, chlorambucil
(celkeran), methotrexate
• Thalidomide has been proven helpful.
• Dapsone and colchicine may be of value in some
cases.
THE PATIENT WITH CHRONIC
MULTIPLE LESIONS
 Pemphigus
• Group of autoimmune, potentially life
threatening diseases that cause blisters and
erosions of the skin and mucous membranes.

Major variants of pemphigus:

• Pemphigus vulgaris- pemphigus vegetans
• Pemphigus foliaceus- pemphigus erythematosus
• Paraneoplastic pemphigus (PNPP)
• Drug-related pemphigus
 PEMPHIGUS VULGARIS

• Autoimmune disease.
• Middle aged females.
• Other variants are:
Pemphius vegetans
Paraneoplastic pemphigus
 PEMPHIGUS VULGARIS
PATHOGENESIS:
• It is an autoimmune disease
• There are circulating antibodies of type IgG.
• These antibodies are reactive against the
desmosomes or the tonofilament complex.
• There destruction or disruption of these
tonofilament complex ,resulting in the loss of
attachment from cell to cell
 loss
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 PEMPHIGUS VULGARIS
CLINICAL FEATURES:
• Painful ulcers or bulla are formed which are
fluid filled.
• any where in the oral cavity .
• The bulla is rapidly ruptured leaving a
collapsed roof of grayish membrane with a red
ulcerated base. The ulcer may look like an
apthous ulcer or may be large map shaped.
• Nikolsky sign is positive.
• Asboe Hansen sign-positive
 PEMPHIGUS VULGARIS
• Sometimes the ulcers are joined together to make a
confluence, this condition is very painful.
• It has a variable course might involve skin,
oesophagus, cervix.
• Protein/fluid, electrolyte and weight loss /secondary
infections.
• Fatal if untreated.
PEMPHIGUS VULGARIS
Oral Findings
• Oral lesions can be the first signs.
• Bulla on a non inflamed base-rapidly break
• Shallow, irregular, large ulcers-edges extend
peripherally-large denuded areas involving most
of the mucosa, co existing candidiasis
• Desquamative gingivitis-sole manifestation
• Thin layer of epithelium peels away in an
irregular pattern, leaving a denuded base.
• Edges of the lesion continue to extend
peripherally
• Buccal mucosa, palate, gingiva, tongue
 DIAGNOSIS

• Skin biopsy
• Electron microscopy has shown that widening
of the intercellular space is followed by
splitting of the desmosome junctions.
• Direct & indirect immunofluorescence
• ELISA
• Laboratory findings and pathology
• Biopsies are best done on intact vesicles and
bullae less than 24 hours old.
• The biopsy specimen should be taken from the
advancing edge of the lesion
• Specimens taken from the center of a denuded
area are nonspecific histologically as well as
clinically.

• Positive nikolsky sign, pressure can be placed on

the mucosa to produce a new lesion; biopsy may
be done on this fresh lesion, taking care to
include the blister base
Direct immunofluorescence
Indirect immunofluorescence
 PEMPHIGUS VULGARIS
Diffrential diagnosis:
• Herpes infection
• RAS
• Acute viral infections
• Severe sunburn of skin
• Desquamative gingivitis
• Pemphigoid
• Erthema multiforme
• Bullous lichen planus
• Candidiasis
TREATMENT:
• Introduction of systemic corticosteroids like
prednisolone in stable cases.
• Prednisolone plus azathioprine methotrexate and
cyclophosphamide in progressed or advanced
cases.
• 1 to 2 mg/kg/d- systemic corticosteroids

Systemic steroids may be lowered in cases of

oral pemphigus by combining topical with
systemic steroid therapy, either by allowing
the prednisone tablets to dissolve slowly in
the mouth before swallowing or by using
potent topical steroid creams.
 Systemic Corticosteroid Regimen I
100 to 120 mg /day
(1.5 mg/kg per day) tapering schedule by
for 2 20 mg per day each dose of 20 mg / day
week
weeks

10 mg per day for reduced to 10 mg

continued for 1
every other day for
month 3 months another 3 months

5 mg
every other day for 6
months
• Cyclophosphamide (cytoxan, mead johnson),
50 to 100 mg orally twice daily
• Azathioprine (imuran, glaxo wellcome), 50 to
100 mg orally twice daily
• Refractory cases- methotrexate, 25 mg /week
• Corticosteroid‐sparing regimen -dapsone, 100
mg/ day +gold sodium thiomalate
• Pulse therapy
• Other therapies- parenteral gold therapy and
dapsone
• Severe recalcitrant cases- intravenous
immunoglobulins, extracorporeal
photophoresis, or plasma exchange
Paraneoplastic Pemphigus (PNPP)
Severe variant, associated with an underlying
neoplasm-
• Non -Hodgkin’s lymphoma
• Chronic lymphocytic leukemia
• Thymoma
• Castleman disease
• Waldenstrom macroglobulinemia
Clinical features
• Adults-60-70 years, both sexes
• Severe, rapid blistering of skin, mucosa
• Pulmonary involvement, conjunctiva, vagina
• Oral lesions-common
• Oral disease is frequently extensive and
painful
• Large, necrotic, painful, inflamed lesions on
lips, tongue, soft palate
 Diagnosis
• History
• Clinical features
• Biopsy
Management
• Treat underlying disease
• Corticosteroids+ azathioprine, methotrexate,
cyclophosphamide
 Subepithelial bullous dermatoses
Group of autoimmune, blistering disorders
characterized by a weakened basement
membrane
• Bullous pemphigoid
• Mucous membrane pemphigoid
• Linear IgA disease
• Epidermolysis bullosa aquisita
• Chronic bullous disease of childhood
 Bullous pemphigoid
Etiology
Subsequent to binding of circulating autoantibodies

complement activation
• Antigens (bp antigens-bp 180 & bp 230)
• Subepithelial vesicle
attracts neutrophils formation
and eosinophils to the basement
membrane zone

release lysosomal proteases

degradation of the basement

degradation of the basement

membrane attachment complex
Clinical features
• Adults, > 60 years
• Macules, papules
• Blister on an inflamed base-scalp, arms, legs,
axilla, groin
• Do not extend at the periphery
• erythematous papular eruption
• Pruritis
• Self limiting
 Oral findings
• 30-50 %
• Vesicles, bullae-small, form slowly, less painful
• Desquamative gingivitis
• soft palate, buccal mucosa, and floor of the
mouth
Differential diagnosis
• Pemphigus
• Mucous membrane pemphigoid
• Lichen planus-bullous, erosive
Management
• Corticosteroids –systemic, topical
• Steroid sparing agents-azathioprine,
cyclophosphamide, mycophenolate
• Dapsone, tetracycline, doxycycline,
minocycline + niacinamide
 Mucous membrane pemphigoid
Cicatricial pemphigoid
• A chronic, autoimmune disorder
• Autoantibodies directed against basement
membrane-subepithelial vesicle formation
• laminin 5 (epiligrin) and a 180-kd protein

• Primarily affects mucous membrane

• Association with underlying malignancy?
Clinical features
• Adults, > 50 years
• Women> men
• Any mucosa, oral mucosa, conjunctiva, laryngeal,
genital, oesophagal, skin
Oral findings
• superficial ulcers
• Desquamative gingivitis
• Vesicles, bullae
• Erosions, ulcerations
• Spread slowly, self limiting
• Scarring on healing
• Nikolsky's sign
• Symblepharon
• Inversion of the eyelashes (entropion)
• Trauma to the cornea (trichiasis)
Differential Diagnosis

• Pemphigus vulgaris
• Erythematous lichen planus
• Linear IgA disease
• Discoid lupus erythernatosus
• Contact allergy
 Management
• Corticosteroids-topical, intralesional, systemic
• Soft splint covering gingiva to hold
medicament
• Tetracycline, doxycycline, minocycline
• Dapsone , immunosuppressants
The Patient with Single
Ulcers
• The most common cause - trauma.
• diagnosis - based on the history and physical
findings.
• Healing should be there within 1- 2 wks.
 Traumatic ulcers
• Direct physical/ mechanical, thermal, or
chemical trauma to the mucosa
• Vascular compromise, causing tissue damage
and ulceration
• Riga- fede disease
• More serious if the mucosa has been
anesthetized and there is prolonged contact
Oral Findings
• Acute ulcerations and necrosis of the mucosa
with a clear antecedent history of injury.
• Yellow-white fibrinous exudate and are
surrounded by an erythematous halo
• Electrical burns- fairly extensive, involve the
lips; initial lesions are charred and dry-
appearing. Sloughs, and there may
be excessive bleeding
• Burns- small and localized to the hard palate
or lips
• Area of tenderness and erythema that
develops into ulcers within hours of the injury.

Differential diagnosis
Laboratory testing
Management
• Surgical correction
• Antibiotics
• Topical anesthetics (such as viscous lidocaine)
• Topical steroids
 Histoplasmosis
• Histoplasma capsulatum
• Fever, malaise, headache, • Children & elders • Mimics chronic TB
• Inhaling
myalgia,pulmonary
symptoms.
dust contaminated
• Hepato &splenomegaly with droppings
• B/L, upper lung
• Bone marrow • Cough, dysponea, wt. loss
• Chest Rg- patchy • Pulmonary Rg
infilteration wid
• Kidney
calcification
Clinical manifestations • GIT &oropharyngeal
ulceration

• Primary infection
Acute is mild,
Progressive Chronic
primary disseminated cavitary
• A self-limiting pulmonary disease that heals to
leave fibrosis and calcification similar to
tuberculosis
• Progressive- cavitation of the lung and
dissemination of the organism
• Immunosuppressed or myelosuppressed patients
Oral findings
• Secondary to pulmonary involvement
• Disseminated form
• HIV associated
• Area of erythema -- papule --- eventually forms a
painful, granulomatous appearing ulcer.
• Cervical lymphadenopathy
• With HIV- ulcer with an indurated border, ; on
the gingiva, palate, or tongue
Differential diagnosis
Squamous cell carcinoma
Infectious etiology
Traumatic ulcerative granuloma
Lymphoma or other malignancy
Laboratory findings
Serology
Antigen detection procedures
Culture
Management
• Immunocompromised- i.V. Amphotericin B
- Itraconazole or
ketoconazole for 6 to 12 months
 Blastomycosis
• Blastomyces dermatitidis
• Not commonly associated with HIV infection

Clinical manifestations
By inhalation- primary pulmonary infection
Acute self-limiting form- asymptomatic
Chronic course- mild symptoms malaise, low-
grade fever, and mild cough
• Untreated- shortness of breath, weight loss,
and production of blood-tinged sputum.
Infection of the skin, mucosa, and bone
• Skin & mucosal lesions- subcutaneous
nodules, slowly progressing to well-
circumscribed indurated ulcers
• Oral lesions are rarely the primary;
concomitant pulmonary lesions

• Nonspecific, painless, verrucous ulcer with

indurated borders; hard nodules and
radiolucent jaw lesions
Differential diagnosis
Chronic oral ulcers
Laboratory findings
• Biopsy and culturing
• Sputum examination, cytology
Treatment
• Ketoconazole, fluconazole, or itraconazole for
mild to moderate disease
• Amphotericin B for severe disease.
 Mucormycosis (Phycomycosis)
• Infection with a saprophytic fungus
• Opportunistic
• Cultured from the human nose, throat, and
oral cavity of healthy asymptomatic
individuals.
Clinical manifestations
• With decreased host resistance
• May appear as a pulmonary, gastrointestinal,
disseminated, or rhinocerebral infection
Rhinocerebral Pulmonary
• TRAID- uncontrolled • Immunocompromised
DM, periorbital
Gastrointestinal pt.
infection, Rare, malnourished • Dysponea, cough,chest
meningoencephalitis Cutaneous pain, fever
• Nose- entry Stomach, colon • Rg- consolidation,
• Blood stained &ileum Trauma- cause cavitation, wedge
discharge, nectrotic Invasive locally shaped infarcts
turbinates Pain, nausea, • Gastrointestinal
• Sinus involvement vomiting, abscess Nectrotic fascites • cutaneous
;later, eye, brain • disseminated
Perforation of
• Facial gangrene
viscus
• Inhalation of the fungus by a susceptible
individual
• Fungus invades arteries and causes damage
secondary to thrombosis and ischemia
• May spread from the oral and nasal region to
the brain
• Proptosis, loss of vision, nasal discharge,
sinusitis, and palatal necrosis
Oral findings
• Ulceration of the palate, which results from
necrosis due to invasion of a palatal vessel
• Lesion- large and deep, causing denudation of
underlying bone
• Gingiva, lip, and alveolar ridge
Differential diagnosis
• Dental pain
• Bacterial maxillary sinusitis
• Aspergellosis
• cellulitis
Laboratory findings
• Difficult to culture from infected tissue
• Biopsy must be performed

Management
Surgical débridement + systemic administration of
amphotericin B (1mg/kg/day) for up to 3 months
Posaconazole- new drug
 References;
• Burket’s oral medicine 11th edn.
• Burket’s oral medicine 10th edn.
• Regzi JA. Oral Pathology clinical pathological correlation 4th edn.
• Cawson RA, Odell EW. Cawson’s essential of oral pathology and oral
medicine 7th edn.
• Robert E. Marx. Oral and Maxillofacial PATHOLOGYA Rationale for
Diagnosis and Treatment 1st edn.
• Ongole R, praveen BN. Textbook of Oral medicine oral diagnosis
and oral radiology.
• Prabhu & Daftary oral disease in tropics
• Norman k wood,paul w goaz,differential diagnosis of oral and
maxillofacial lesion,fifth edition.