Ulcerative, vesicular

and bullous lesions

Dr . Zainab Hasan
Ulcerative, vesicular and bullous
lesions :
1- onset of the lesion.
2- duration of the lesion.
3-recurrence or progression of the lesion.
4-presence of vesicles preceding ulcers.
5-presence of skin ,eye, genital lesion.
6- association of oral ulcers and systemic
manifestation.
7-medications.
Dermatologic lesion are classified
according to their clinical appearance:
1-macules
2- papules
3-plaques
4-nodules
5-vesicles
6-bullae
7-erosive
8-pustules
9-purpura.
Classification:
1- acute multiple lesions.
2-recurring oral ulceration.
3-chronic multiple lesion.
4- single ulcer.
Acute multiple lesions:
1-viral infection.
2- EM
3-allergic stomatitis.
4-oral ulcers secondary to cancer
chemotherapy.
5-ANUG
1 - Viral infection
Primary hereps simplex (primary hereptic
gingivostomatitis)
General symptoms fever , headache .malaise,
nausae ,vomiting and tender
lymphadenopathy.
Oral manifestation vesicles ,shallow ,round
ulcer and generalized acute marginal
gingivitis and the entire gingiva is edematous
and inflamed.
treatment:
1 supportive care which include
analgesic ,fluid to maintain proper hydration
and electrolyte balance and topical
anesthesia prior
2 cyclovir (zoverax) 200 mg 1x4 daily for 5
days.
2- varcicella – zoster virus infection
Vzr responsible for 2 major clinical infection:
chicken pox (varicella) and shingles (herpes
zoster).
Herpes zoster:
Prodromal period of 2-4 days,shooting pain,
parasthesia , burning and tenderness along
the course of affected nerve.
Unilateral vesicles on an erythematous base
along the course of nerve (trigeminal nerve)
then vesicles scabs in one week and healing
take place in 2-3 weeks.
Post herpetic neuralgia: characterized by
continuous pain for weeks to month after
herps zoster or become chronic and occurs
most frequently in elderly patients as a result
of scarring of the nerve.
Ramsay hunt syndrome: hereps zoster
affected geniculated ganglion (motor
nerve)characterized by Bell’s palsy ,unilateral
vesicles of external ear , vesicles of oral
mucosa.
treatment:
Mild case (young healthy individuals) use
acyclovir 200 mg 5 times daily.
Elderly people use prednison 40-60 mg for 1-2
weeks to prevent post herpetic neuralagia.
Coxsackie virus infection:
1-Herpangina
Systemic manifestation: fever,chills,anorexia
and lymphadenopathy.
Oral manifestaion: vesicles and ulcers
involving soft palate and tonsillar pillars, sore
throat, dysphagia and sore mouth.
Herpangina clinically distinguished
from primary HSV infection by:
Herpangina is epidemic.
Lesions of herpangina occur on the pharynx
and posterior portion of oral mucosa ; where
as HSV infection affect the anterior portion of
oral cavity.
Herpangina doesn’t cause generalized acute
gingivitis like HSV infectins.
Lesion of herpangina tend to be smaller than
HSV infections.
2-Hand,foot and mouth disease:
characterized by low grade fever,oral vesicles
and ulcers of hard palate,tongue and buccal
mucosa and non-pruritic macules, papules
and vesicles on the extensor surfaces of hand
and feet.
2-Erytheme multiforme:
Is an acute inflammatory disease of the skin
and mucous membrane,the most
characteristic feature is the iris or target
lesions of the skin , with central vesicles
surrounded by concentric erthymatous and
skin colored ring.
The most cutaneous area involved hand ,
feet, and extensor surfaces of elbow and
knees.
Oral ulcers are most commonly located on the
lips,buccal mucosa and tongue.
Stevens –johnson syndrome:
is sever form of EM characterized by vesicles
and bullae involve skin, mouth , genitalia.
Etiology:
Durgs (sulfonamide , phenobaraital and
pencilline).
M.O (HSV ,mycoplasma pneumoniae).
Stress and emotional factors.
Radiotherapy.
crohn’s disease.
Bengin and malignant tumors.
Idiopathic.
3-Allergic stomatitis:
Ab-Ag reaction cause anaphylactic or immediate
type hypersenstvity reaction characterized by
erythema ,edema , such as urticaria and
angioneurotic edema , multiple vesicles and
ulcers of oral mucosa , or a lichenoid reaction
associated with burring sensation.
Stomatitis medicamentosa: the reaction may
result from a systemic administrated Ag as a
reaction to barbiturate .
Contact stomatitis : the reaction result from
topical Ag as acrylic denture , tooth paste,
chewing gum, dental amalgum ,gold crown.
Oral lesion occur less frequently ‫؟؟؟‬
than skin lesion due to
4- oral ulcer secondary to cancer
chemotherapy:
Indirectly: depress the bone marrow and
immune response to bacterial , viral , fungal
infections.
directly: effect on the replication and growth
of oral epithelial cell by interfering with
nucleic acid and protein synthesis of oral
mucosa which lead to thinning and ulceration
of oral mucosa.
5- Acute Necrotizing Ulcerative
Gingivitis ANUG
Is an endogenous oral ulceration
characterized by necrosis of gingiva. The
organisms cause are anaerobic fusiform
bacteria and spirochaetes.
Typical lesions consist of necotic punched out
ulceraration on interdental papillae and
marginal gingiva.
predisposing factors :
Poor oral hygiene .
Smoking
Emotional stress
Leukemia or plastic anemia
AIDS.
Treament:
1- hygiene instruction.
2- hydrogen peroxide 1x3 daily and
chlorehexidine mouth wash.
3- metronidazole 200 mg 1x3 a week and
penicillin.
Recurring oral ulcer :
Recurrent aphthus stomstitis.
Bahcet’s disease.
Recrrent herpes simplex virus infection.
Recurrent aphthous stomatitis :
Oral ulceration divided into:
Minor oral ulceration.
1-the ulcers are less than 10 mm in diameter.
2-heal without scarring.
3- heal with in 7-10 days.
4- shallow , round oval ulcers have a grey
yellow base with an erythematous margin,
affect the non keratinized area of oral mucosa
. Most common site buccl and labial mucosa .
Major oral ulceration
1- the ulcer greater than 10 mm in diameter .
2- heal with scarring .
3- heal with 4-6 weeks .
4-affect the keratinized areas of the oral
mucosa .
Herpetiform oral ulceration
1- small, pin-head sized ulcers 1-2 mm
Heal without scarring.
Heal within 2-3 weeks.
4- occur at any part of oral mucosa .
Etiology:
Hereditary predisposition HLA- B12 , HLA-
D77
Trauma
Emotional stress
Infective agents (HSV ,
VZV ,cytomegalovirus , streptococcus sangius
,alllergic disorder
Hematological disorder
Gastrointestinal diseaess
Hormonal disturbance
Treatment:
Treat the underlying predispoising factors
Medication :
Mild – moderate topical corticosteriod .
More sever : systemic coticosteroid or
interlesion steroid injection .
Bahcent’s disease :
Is an idiopathic disorder characterized by classical
triad of RAS of any types including recurring oral ulcer
,genital ulcers ,eye lesions and system disorder.
Etiology:
Immunologic abnormalities.
Genetic HLA-B51
Environmental pollutants and M.O
Diagnosis : recurrent oral ulceration occurring at least
3 times in a year and 2 of following 4 manifestation :
Recurrent genital ulceration.
Eye lesion
Positive pathergy test
Skin lesion .
treatment:
Combination immunosuppressive and
systemic corticosteroid such as azathioprine
and prednisone .
Combination of cyclosporine or cholchicine
with corticosteroid .
3- Recurrent herpes simplex virus
infection
Recurrent herpes labials occur in patient who
have experienced aprevious herpes simplex
infection and have serum antibody protection
against another exogenous primary infection.
Recurrent is not reinfection but reactivation of
virus that remain latent in nerve endings.
Precipitatation factors are:
Trauma to lips
Fever . Sun burn
Mensturation.
Dental extraction
Low serum IgA.
Treatment:
Oral acyclovir prevent recurrence can use as
a prophylaxis when patients experience sever
lesions after sun exposure.
Topical a cyclovir has not a significant but
used to decrease healing time and relief
pain but not prevent recurrence.
Chronic multiple lesions
1-pemphigus .
2- bullous pemphigoid .
3- erosive and bullous lichen planus.
1-pemphigus vulgaris:
Is an autoimmune disease involving the skin
and mucosa charcterized by intraepithelial
bullae formation. It caused by antibodies to
intercellular cementing substances lead to
loss of intercellular substance in the lower
layers of stratum spinosum followed by
widening of intercellular spaces , destruction
of desmosomes and finally cellular
degeneration.
The separation of cells called acantholysis
which result in suprabasilar bulla.
Etiology :
Coexisting with other autoimmune disease
myasthenia gravis and other multiple
autoimmune diseases.
Drug therapy
Diagnosis :
1- biopsy (intraepithelial bulla)
2- cytologic examination T- Zank smear
3- immunofluorescent.
3-Erosive and bullous lichen planus
Occur in sever form of disease when
extensive degeneration of basal layer of
epithelium caused separation of epithelium
from underlying CT.
In some cases the lesion will start as vesicles
or bullae classified as bullous lichen planus .
Etiology:
Drug therapy (NSAI ,pencillinamine .
Hydrochlort ,dental restoration)
Liver disease( chronic cirrhogenic , hepatitis)
Graft versus host disease
Stress , smoking.
Single ulcer :
Traumatic ulcer .
Infections : fungal
SCC