This document discusses vesiculobullous lesions, which are elevated fluid-filled blisters on the skin or mucosa that are either vesicles (less than 1cm) or bullae (greater than 1cm). It covers the classification, etiology, pathogenesis, clinical features, diagnosis and management of various conditions that cause vesiculobullous lesions, including herpes simplex virus infections, varicella zoster virus infections, herpangina, hand foot and mouth disease, and more. Key points include how these viruses cause primary infection and can later reactivate to cause characteristic lesions, as well as how their oral manifestations, complications, and treatments are described.

1. VESICULOBULLOUS
LESIONS
ASEEM MOHAMMED
FINAL YEAR PART 1

2. VESICULOBULLOUS LESIONS
 VESICLES: Elevated blisters containing
clear fluid that are less than 1cm in
diameter.
 BULLAE: elevated blisters containing clear
fluid that are greater than 1cm in diameter

3. VESICLE

4. BULLAE

5. CLASSIFICATION
1. HEREDITARY LESIONS
 Familial benign chronic pemphigus
 Epidermolysis bullosa
2. VIRAL LESIONS
 Herpes simplex virus infections
 Varicella zoster virus
 Herpangina
 Hand foot and mouth disease
 measles

6.  IMMUNOLOGICAL LESIONS
 Pemphigus
 Pemphigoid
 Erythema multiforme
 Linear IgA disease
 Allergic stomatitis

7. HERPES SIMPLEX VIRUS INFECTIONS
 All herpes virus contain DNA nucleus which
can remain latent in host neural cells
thereby evading host immune response
 ETIOLOGY AND PATHOGENESIS
 HSV1- infections above the waist
 HSV2- infections below the waist
 Both HSV 1 and HSV 2 can be transmitted
sexually

8.  The primary infections is acquired by
inoculation of mucosa skin and eye with
infected secretions
 The virus then travels along the sensory
nerve axons and establishes chronic latent
infections in the sensory ganglion.

9.  Most common sites are oral mucosa, genital
mucosa and eyes
 HSV infection of cornea is the major cause of
blindness
 Herpes whitlow:an infection of the fingers when
virus is inoculated into the fingers through a
break in the skin
 Common occupational hazard in dental
professional

10. CLINICAL MANIFESTATIONS
 PRIMARY GINGIVOSTOMATITIS:
 Usually occur in children and teenagers
 fever,loss of appetite , malaise and
myalgia, headache and nausea.
 The disease is self limiting and resolves
within 10-14 days

11. ORAL FINDINGS
 After a few days, erythema and clusters of
vesicles appear on the keratinized mucosa of
the hard palate , attached gingiva and
dorsum of the tongue and non keratinized
mucosa of the buccal and labial mucosa,
ventral tongue and soft palate.
 Vesicles break down to form ulcers that are
usually 1 to 5 mm and coalesce to form
larger ulcers with scalloped borders and
marked surrounding erythema.

13.  The gingiva is often red and the mouth is
extremely painful causing difficulty in
eating.
 Pharyngitis causes swallowing difficulties.

14.  RECRUDESCENT ORAL HSV INFECTIONS:
 Reactivation of HSV may lead to
asymptomatic shedding of HSV in the
saliva and oral secretions ,which is an
important risk factor in transmission.
 The term recrudescent HSV refers to the
actual ulcerations caused by reactivated
virus

15.  Fever , ultraviolet radiation, trauma,stress,
menstruation are important triggers for
reactivation of HSV.
 Recrudescent HSV on the lips is called
recurrent herpes labialis
 symptoms-itching, tingling or burning
followed by the by the appearance of
vesicles,ulcers,crusts
 Pain-present only with in first 2days

18.  RECURRENT INTRAORAL HSV(RIH)-Intra oral
recrudescent HSV in the
immunocompetant host occurs chiefly on
the keratinised mucosa of the hard palate
,attached gingiva, and dorsum of the
tongue.
 They present as 1 to 5 mm single or
clustered painful ulcer with a bright
erythematous border.

19.  One common presentation is the
complaint of pain in the gingiva 1 to 2
days after a scaling and prophylaxis or
other dental treatment.
 HSV in Immunocompromised
patients-patients who are undergoing
chemotherapy . Who have undergone
organ transplantation,or patients suffering
with AIDS ,RIH may occur in any site
intraorally.

20.  If undiagnosed and left untreated RIH
infections may disseminate to other sites
and cause severe infections in the
immunocompromised patients.
 DIFFERENTIAL DIAGNOSIS
1. HAND FOOT AND MOUTH DISEASE
2. HERPANGINA
3. Necrotizing ulcerative gingivitis
4. Recurrent aphthous ulcer

21.  ERYTHEMA MULTIFORME- It occur in
young adults as compared to herpes
simplex which occurs in children.

22. LABDIAGNOSIS
 HSV isolation by cell culture is the gold
standard test for the diagnosis.
 advantage- high sensitivity and specificity
 The disadvantage- need specialised
equipment , is expensive, and may take
upto several days for a final result.

23.  Recently polymerase chain reaction from
swabs has been shown to detect antigen 3
to 4 times more common than culture.
 HSV can be identified from scrapings from
the base of lesions smeared onto glass
slides.
 These can be stained with Wright, Giemsa
or Papanicolaou stain to demonstrate the
characteristic multinucleated giant cells or
intranuclear inclusions.

24.  Primary HSV infections is associated with
elevated immunoglobulin IgM titers
followed several weeks later by permanent
IgG titers that indicate previous infection
but confer no protection against
reactivation.
 Recurrent infection is associated with the
rise in IgG antibody titer in acute and
convalescent sera.

25. MANAGEMENT
 PRIMARY HSV INFECTION:
 Management is directed towards pain
control , supportive care, and definitive
treatment
 PAIN CONTROL AND SUPPORTIVE CARE
MEASURES –
 2% Viscous lidocaine(swish and spit out
5ml 4-5 timesday)
 Liquid diphenhydramine (swish and spit
out 5 ml 4 to5 timesday

26.  Combination of viscous lidocaine
,diphenhydramine and a covering agent
such as kaopectate or maalox)in 1:1:1
ratio.
 Benzydamine
 Systemic analgesia
 SUPPORTIVE CARE:
 Hydration
 Ice chips

27.  Soft balanced diet
 Antipyretics such as ibuprufen as needed.
 Aspirin is contraindicated in children with
viral illness has been associated with
Reye’s syndrome ,a potentially fatal
condition characterised by fatty
degeneration of the liver and
encephalopathy.

28.  Antiviral drugs such as acyclovir 15mg/kg
5 times a day in children reduces the
duration of fever , reduces HSV shedding
,halts the progress of lesion , improves
oral intake.
 Valacyclovir the prodrug of acyclovir has 3
to 5times the bioavailability of acyclovir.

29.  RECCURENT HSV-
 RHL can be suppressed by reducing trigger
factors such as by using sunscreens.
 Antiviral medications reduces shedding,
infectivity, pain and the size and duration of
lesion.
 5%acyclovir cream,3%penciclovir cream and
10% docosanol cream are effective if applied
3 to 6 times a day at first prodrome or sign
of lesion

30.  HSV IN IMMUNOCOMPROMISED PATIENTS:
 systemic antivirals to prevent dissemination
to other sites.
 Acyclovir and valacyclovir suppress HSV
reactivation who are HSV seropositive
 Acyclovir resistant HSV is most frequently
seen in this group of patients where the
virally derived thymidine kinase that activate
acyclovir is mutated. here foscarnet is the
drug of choice.

31. Varicella zoster virus infections
 Etiology and pathogenesis-
 Primary infection with VZV leads to the
chicken pox(varicella)
 The virus then becomes latent usually in
the dorsal root ganglia or ganglion of the
cranial nerves.
 Reactivation produces herpes zoster
infection(HZI) commonly called as shingles

32.  The incidence of HZI increases with age
and degree of immunosuppression
 This virus is cytopathic to epithelial cells of
skin and mucosa causing blisters and
ulcers.
 Transmission –respiratory route
 Incubation period-2 to 3 weeks

33. CLINICAL FINDINGS
 VARICELLA ZOSTER-
 PRIMARY VZV- occurs in the first 2
decades of life.
 Low grade fever, malaise and
development of an intensely pruritic
maculopapular rash, followed by vesicles
which is ‘dew drop like’.
 These vesicles turn cloudy and pustular
burst and scab with crusts falling off after
1 to 2 weeks.

36.  Lesions begin on trunk and face and
spread centrifugally.
 COMPLICATIONS-
 Cerebellar ataxia
 Encephalitis
 Pneumonia
 Myocarditis
 Hepatitis

37.  HERPESZOSTER INFECTIONS-
 more common in adults,start with deep
aching or burning pain
 Little or no fever or lymphadenopathy
 Appearance of crops of vesicles in a
dermatomal or zosteriform pattern in 2 to
4days
 This pattern describes the unilateral linear
and clustered distribution of vesicles, ulcers
and scabs in a dermatome supplied by one
nerve

40.  Lesions heals with in 2 to 4 weeks with
scarring and hypopigmentation.
 Occasionally HZI may occur without the
appearance of dermatosomal lesions
which makes the diagnosis challenging
and the patients present with facial palsy.

41.  COMPLICATIONS
 Postherpetic neuralgia
 Acute retinal necrosis
ORAL MANIFESTATION
 Primary VZV infection presents as minor
acute ulcerations in the mouth.
 In recurrent VZV the ophthalmic division of
trigeminal nerve is the cranial nerve most
often affected.

42.  Corneal involvement may lead to
blindness.
 Involvement of this nerve leads to lesions
on the upper eyelid , fore head and scalp
with v1.
 Midface and upper lip with V2 and lower
face and lower lips with v3
 With involvement of v2 patients have pain
burning and tenderness usually on the
palate on one side

43.  Then appearance of painful ,clustered 1 to
5mm ulcers on the hard palate or buccal
gingiva in a unilateral distribution
 Ulcers heal with 10 to 14 days

44.  HERPERZOSTER INFECTIONS
 resorption and exfoliation of teeth and
osteonecrosis of jaw bones especially in
patients with HIV disease.
 An uncommon complication of HZI –
Ramsay Hunt Syndrome .
 Patients develop bells palsy ,vesicles of
the external ear and loss of taste
sensation in anterior 2 third of the tongue.

45.  DIFFERENTIAL DIAGNOSIS-
 PULPITIS-
 The pain experienced before the onset of
vesicles and ulcers may lead to incorrect
diagnosis.
 HERPES SIMPLEX INFECTION
 Culture can differentiate between two.
 PEMPHIGUS AND PEMPHIGOID-
 They are not present unilaterally

46. LAB FINDINGS
 Viral isolation using cell culture
 Direct fluorescent antibody testing using a
smear have greater sensitivity.
 This test uses a smear obtained by
scraping the lesion and staining with
antibody against VZV conjugated to a
fluorescent compound.
 After primary infection the patients sero
converts and IgA against VZV is detectable
in the serum

47. MANAGEMENT
 Pain control , supportive care and hydration
,minimizing the risk for dissemination.
 Ibuprofen is preferred analgesic
 Treatment for primary VZV infections
 Acyclovir – 800mg 5 times daily
 Herpes zoster
 Valacylovir – 1000mg 3 times daily for 7 days
 Famciclovir – 500mg 3 times daily for 7 days
 This should be treated within 72hrs of
disease onset

48.  Postherpetic neuralgia
 First line treatment-gabapentin and 5%
lidocaine patch
 Second line treatment-opioid analgesics
and tricyclic anti depressents

49. PREVENTION
 VZV-A live , attenuated vaccine reduces the
incidence of varicella outbreaks.
 Vaccination of older adults with this vaccine
causes-
 Increase in antibody levels
 Boosts cell specific immunity
 Reduces incidence and severity of HZI
 Reduces post herpetic neuralgia.

50. COXSACKIE VIRUS INFECTIONS
 HERPANGINA
 The word herpangina derives from herpes
meaning “vesicular eruptions” and angina
meaning “inflammation of the throat”
 Its caused by coxsackie virus A 1-10
,CVA16 and CVA 22
 Transmission-ingestion,Direct
contact,droplet spread

51. CLINICAL FINDINGS
 Children under 10yrs usually affected and
occur in epidemics in summer
 Incubation period-2-10 days
 Fever, headache,vomiting,abdominal pain
 ORAL MANIFESTATION
 First oral symptoms- sore throat and pain on
swallowing
 Erythema of oropharynx, soft palate and
tonsillar pillars.

53.  Small vesicles are formed but they rapidly
breakdown to 2 to 4 mm ulcers . They
persist for 5 to 10 days.

54. Lymphonodular pharyngitis
 Variant of herpangina and associated with CVA 10.
 Clinical features:-
 Age-children,young adults
 Site-uvula,soft palate,post.orophaynx
 Incubation period-2-10days
 Patient report with a sore throat,elavated temp,mild
headache,anorexia
 Yellowish white nodules surrounded by zone of erythema
 Patient develop diffuse small nodules in the oropharynx
 Lesion do not produce vesicles or do not ulcerate
 Lesion resolves with in 6-10 days
 No Rx required ,disease is self limiting

55.  HAND FOOT AND MOUTH DISEASE
 CVA16 is the most common cause
 CVA7, CVA9, CVA10, CVA24. CVB2, CVB5
 Entero virus (EV71) is a common cause of
HFM disease.
 HFM tends to be seasonal occurs in
epidemic , clusters and has high
transmission rates

56. CLINICAL FINDINGS
 HFM usually affects children younger than
10 yrs.
 Low grade fever and sore throat.
 75 to 100% patients have skin rash
especially on the hands and feet and 30%
on buttocks.
 The rash is first red and macular and
becomes vesicular.

60. ORAL MANIFESTATIONS
 Patients are febrile and complains of sore
mouth and throat.
 Lesions begin as erythematous macules
that becomes vesicles and quickly
breakdown to ulcers.
 Lesions are located on the tongue, hard
and soft palate and buccal mucosa.

62. DIFFERENTIAL DIAGNOSIS
 1.Primary HSV:-
 Lesions in palms and soles are typical for
hand foot and mouth.
 Ulcers in posterior oral cavity are typical
for herpangina
 Bright red and painful gingivacan be seen
in primary HSV and its uncommon in CV.
 Herpangina and HSV

63.  2.Chicken pox-ulcers are not prominent in
oralcavity,generalised vesicular skin lesions seen
 3.Streptococcal infections of throat:- do not
produce vesicles or ulcers

64. LABORATORY FINDINGS
 CVB- diagnosed by culture
 CVA16- grow rapidly
 CVA is best identified by inoculation into
newborn mice.
 Reverse transcriptase PCR –sensitive and
rapid way of identifying viral RNA in
clinical specimen.

65.  Diagnosis is usually made on clinical findings and
cultures and biopsies are rarely necessary.
 Skin biopsies of HFM and HERPANGINA show
intraepidermal vesicles with a mixed lymphocytic
and neutrophilic infiltrate, degeneration of
epidermal cells and dermal edema.
 Eosinophilic nuclear inclusions and
intracytoplasmic picornavirus particles are seen
in surrounding dermal vessels.
 Biopsy of lymphonodular pharyngitis shows
hyperplastic lymphoid nodules.

66. MANAGEMENT
 CV infections are self limiting
 Management is directed towards control of
fever and mouth pain , supportive care.
 Limiting contact with others to prevent
spread of infections.
 Effective antiviral agents for CV are not
available.

67. MEASLES

68. MEASLES
 Also called as rubeola or morbilli
 Acute contagious viral infection
 Primarily affecting children
 Occur in epidemic form
 It is caused by paramyxovirus

69. Transmission
 Direct contact with a person
 Droplet infection

70. Clinical features
 Incubation period-8 to 10 days
 Symptoms:-fever,malaise,cough,conjuctivitis,phot
ophobia,lacrimation,eruptive lesions of skin and oral
mucosa,sore throat
 Skin- skin eruption begins on face,in the hairline, behind
the ear and spread to neck,chest,back and extrimities
 Appearance-tiny red macules or papules enlarge and
coalesce to form discolored irregular lesions which
blanch on pressure
 Fade away in 4to 5 days with fine desquamation

72. Oral manifestations
 Oral lesions precede 2to 3 days before cutaneous rash
 Site- buccal mucosa
 Intraoral lesions-kopliks spots – occur in 97% of cases
 Appearance-small irregularly shaped flecks which appear
as bluish white specks surrounded by bright red margins
 Signs-generalised inflammation,congestion,
swelling,focal ulceration of gingiva,palate and throat
 Increase in no. and coalesce to form small patches

74. Complications
 Bronchial asthma
 Encephalitis
 Noma
 Hodgkins lymphoma
 Induction of remission of leukemia
 Otitis media

75. Differential diagnosis
 Smallpox-high fever,monoform exanthema
 Chickenpox-typical exanthema that follows
intraoral lesion

76. management
 The patient should be isolated
 Vitamin A should be given
 Ribavirin- 20-30 mg/kg-IV for 7days
PREVENTION
 Active immunisation-one injection of live attenuated
measles vaccine(MMR vaccine) –subcutaneously in
children over one year
 Passive immunisation-human immunoglobulin-IM-
under 18 months of age and debilitated children
 DOSE
250 mg-children under 1 year
500 mg-over 1 year

77. EPIDERMOLYSIS
BULLOSA

78. EPIDERMOLYSIS BULLOSA
Definition:
 A large group of clinically similar
desquamating disease processes of the
skin and mucosa that have in common the
separation of the epithelium from the
underlying connective tissue and the
formation of large blisters that frequently
result in extensive and often immobilizing
scar formation.

79. classification
1. Epidermolysis Bullosa Simplex
-generalised form
-localised form
2. Dystrophic Epidermolysis Bullosa
-dominant
-recessive
3. Junctional Epidermolysis Bullosa

80. Clinical features
1. Epidermolysis Bullosa Simplex
Generalised form
 Age-inherited as autosomal dominant trait
 Manifests at birth
 Vesicle or bullae-Sites of trauma/friction
 Involve hands and feet. neck, knees and elbow are
rarely affected
 Healing- with in 2 to 10 days, no scarring or
pigmentation seen
 Prognosis-good and disease appears to improve at
puberty
 Localised form-limited to hands and feet only and
exacerbate in hot weather

82. Epidermolysis bullosa dystrophic
dominant
 Age-onset at infancy and delay until
puberty
 Sites-blister develop on
ankles,knees,elbows,feet and head.
 Healing-results in scarring
 Signs-hair may be sparse, nails are thick
and dystrophic

84. Epidermolysis bullosa dystrophic
recessive
 Age-onset at birth
 Formation of bullae spontaneously,sites of
trauma,friction or pressure
 Sites-feet, buttock,scapula,elbows,finger
 bullae contains a clear,bacteriologically sterile or
blood tinged fluid
 when bullae rupture under trauma or
pressure,they leave raw, painful surface
– Nikolskys sign- positive
 Healing-heal by scar formation

85. junctional Epidermolysis
Bullosa
 Severe form of dystrophic recessive type
 Onset at birth
 Absence of scarring,pigmentation and
death within three months of age
 Bullae similar to recessive
 Develop simultaneously and sheets of skin
may be actually shed

87. 0ral manifestations
 Epidermolysis Bullosa Simplex
 Bullae of oral cavity can be seen in
generalised EB
 Teeth are not affected

88.  Bullae can occur sometimes
 Teeth are unaffected
Epidermolysis bullosa dystrophic
dominant

89. Epidermolysis bullosa dystrophic
recessive
 Oral bullae are common
 Prodromal signs:-
 preceded by white spots or patches on oral
mucosa or by development of localised areas of
inflammation
 bullae are painful when rupture or when
epithelium desquamates
 Scar formation- results in restriction of tongue
movement
 Hoarseness and dysphagia due to bullae
of larynx and pharynx

90.  Teeth:-defects seen like:-
 -rudimentary teeth
 -congenitally absent teeth
 -hypoplastic teeth
 -crowns denuded of enamel

91. junctional Epidermolysis
Bullosa
 Oral bullae are very extensive
 Due to extreme fragility ,causes serious
feeding problems
 Deciduous teeth-disturbance in enamel
and dentin formation

92. Diagnosis
 Diagnosis is simple when the family
history,reaction to trauma are taken into
consideration

93. management
 Large blisters should be pricked and blister
fluid released
 Dressing to minimise reaction may be
helpful
 Topical antibacterial agents:-apply to the
affected area
 bacitracin/neomycin
 sulfadiazine silver 1%
 mupirocin 2%

94.  Aluminim chloride topical 20%
Antibiotic:-
 Tetracycline-250-500mg orally every 6hrs

95. REFERENCE
 BURKETS ORAL MEDICINE
 SHAFERS TEXTBOOK OF ORAL
PATHOLOGY
 TEXTBOOK OF ORAL MEDICINE-ANIL
GHOM
 INTERNET

96. THANKYOU