Oral ulcers

Oral ulcers
Classification
I. oral ulcers may classify to primary and secondary ulcers
a. Primary ulcers: which are not preceded by vesiculo-bullous lesion
• Traumatic ulcer
• Infective: bacterial and fungal infection
• Neoplastic
• Systemic: GIT and blood disorders
• Aphthous
• Behcet’s syndrome
• Reiter’s syndrome
b. Secondary ulcers: which are preceded by vesiculo-bullous lesion
i. Intra-epithelial vesicles
a. Non acantholytic lesions (death and rupture of groups of epithelial cells)
- Herpes simplex
- Herpes zoster
- Herpangina
- Hand, foot and mouth disease
b. Acantholytic lesions (destruction of intercellular attachment)
- Pemphigus vulgaris

ii. Subepithelial vesicles:

- Bullous pemphigoid
- Mucous membrane pemphigoid
- Erythema multiform
- Bullous lichen planus
- Epidermolysis bullosa
- Drug eruption
- Linear IgA diseases
II. Oral ulcers may be classified according to etiology
1. Physical and chemical agents (reactive ulcers):
• Traumatic, thermal, chemical, electrical and radiation
2. Microbial agents:
a. Bacterial:
- Necrotizing ulcerative gingivitis
- Tuberculosis
- Syphilis

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b. Fungal:
- Histoplasmosis
- Blastomycosis
- Coccididomycosis
- Cryptococccosis
c. Viral:
- Herpes simplex
- Herpes zoster
- Herpangina
- Hand, foot & mouth disease
3. Neoplasm: SCC
4. Immunological reactions:
- Aphthous ulcers
- Behcet’s syndrome
- Pemphigus vulgaris
- Mucous membrane pemphigoid
- Lupus erythematous
- Lichen planus
- Epidermolysis bullosa
- Drug eruption
5. Blood disorders:
- Anemia
- Leukemia
- Neutropenia
6. Gastrointestinal disease:
- Coeliac disease
- Ulcerative colitis
- Crohn’s disease
7. Drugs:
• Cytotoxic drugs

I. Reactive oral ulcers:

These ulcers are due to: trauma, thermal, radiation & electrical
1. Mechanical trauma:
Traumatic ulcers may be attributed to:
a. Accidental trauma: sudden biting, trauma may occur during epileptic seizures or
sudden blow where the soft tissues are trapped between the teeth.
b. Self-induced trauma via abnormal habits as cheek or lip biting

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c. Iatrogenic (induced by dentist): during dental treatment soft tissue injury may be
induced via dental instruments, negative pressure of saliva ejector or rapid and forceful
removal of cotton rolls ‘’ cotton roll stomatitis’’
d. Ulcers of lingual surface of the tongue in neonates induced during sucking by trauma
of lower incisors
e. Dentures may be associated with ulcers which are either acute (sore spots), or chronic
ulcers.
f. Biting on lips & cheek after local anesthesia

N.B.
Most ulcers of local cause have an obviousaetiology, are acute, usually single ulcers, lastless
than three weeks and heal spontaneously.Chronic trauma may produce an ulcer with akeratotic
margin.
2. Chemicals ulcer
Chemicals may induce oral ulcers because of their:
a. PH value (acidic or basic)
b. Antigenic reaction
Treatment: symptomatic treatment
a. Benzdiamine hydrochloride (anti-inflammatory mouth wash)
b. Topical steroid
c. Tetracycline mouth bath if there is secondary infection

II. Microbial agent ulcers

❖ Bacterial agents
1. Necrotizing ulcerative gingivitis:
It is an inflammatory destructive disease of the gingiva which is characterized by:
a. Punched out, crater like depression at the crest of the interdental papilla (IDP)
b. Pseudomembranous slough covering the gingival crater
c. Linear erythema demarcating the affected tissue from the remainder of the gingival
mucosa
d. The lesion may extend from interdental papilla to marginal & attached gingiva and the
bone may be exposed
e. The tissue (tongue, cheek & lip) in contact with diseased gingiva may be involved
Smear from the lesions present scattered bacteria, predominantly spirochetes and fusiform
bacilli.
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Treatment
1. 3% H2O2 and warm water rinsing every 2 hours
2. 0.2 % chlorohexidine solution twice daily
3. Antibiotics in case of systemic manifestations
a. Metronidazole 250mg 3times daily
b. Penicillin 250mg 4 times daily for 3-5 days
c. Tetracycline 250mg 4 times daily for 4 days
4. Oral hygiene measures, proper scaling and patient’s motivation

2. Tuberculosis
It is a disease caused by mycobacterium tuberculosis and is characterized by granuloma formation
in any organ in the body but usually affects the lungs.
Oral lesions secondary to pulmonary tuberculosis and frequently begin as small tubercles that
break down to form painful ulcers. The ulcer commonly involves the tongue and characteristically
is:
Chronic painful, indurated ulcer with irregular undermined edge and thick mucous material in the
base.
3. Syphilis
Syphilis is caused by the spirochete Treponema pallidum. It is acquired by sexual contacta partner
with active lesions, by transfusion of infected blood, or by transplacental inoculation of the fetus
by an infected mother. and is characterized by numerous systemic manifestations that appear in
three general stages over months to years.
1. Primary syphilis:
- Chancre, a chronic ulcer at the site of infection, painless, indurated ulcer(s) with raised
margins and does not produce an exudate at the site of inoculation.
- Regional lymphadenopathy, firm, painless swelling.
- The lesion heals without therapy in 3 to 12 weeks, with little orno scarring.
2. Secondary syphilis
- Oral mucous patches, condylomalatum, maculopapular rash.
- In untreated syphilis, secondary disease begins after about 2 to 10 weeks. The spirochetes
are nowdisseminated widely and are the cause of a reddish brown maculopapular cutaneous
rash
- Mucosalulcers covered by a mucoid exudate.
- Elevated broad-based verrucal plaques, knownas condylomatalata, may also appear on the
skin and mucosal surfaces.
- Inflammatory lesions may occurin any organ during secondary syphilis.
3. Tertiary syphilis (gumma):

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- Gumma start as small, firm nodular mass enlarge to several centimeters in diameter,
followed by necrosis and produce oral ulceration
- It is painless sharply demarcated punched out ulcer
- Healing after several months
- The oral lesion of tertiary syphilis is non-contagious and most frequently involves the
palate and tongue
Palate:gummatous destruction of the palatal bones is a known cause of perforation of the palate
Tongue: chronic ulcerated gumma manifests as: solitary, deep, punched out ulcers

4. Deep fungal infection

Histoplasmosis (HistoplasmaCapsulatum), Coccidioidomycosis (CoccidioidesImmitis),
Blastomycosis (BlastomycesDermatidis) &Cryptococcosis (Cryptococcus Neoformans)
Clinical features
- These fungi primarily involve the lunge (mimic TB)
- The reservoir is in soil contaminated by avian droppings, especially from pigeons and
chickens the disease is transmitted by inhalation of airborne spores
- The manifestations include cough, fever, night sweat and +/- weight loss
- 95% of histoplasmosis is either subclinical or present as mild respiratory illness
- In the other 5% of cases the disease has an acute or chronic progressive course with
dissemination to the spleen, liver, lymph nodes adrenals and bone marrow
- Blastomycosis may induce clinical features similar to cervicofacialactinomycosis with
multiple draining sinuses
- Coccidiomycosis may induce skin eruption similar to EM
Oral manifestations
Oral lesions are secondary to
a. Implantation of the oral mucosa by infected sputum
b. Hematogenous spread secondary to erosion to erosion in pulmonary vessels due to
inflammatory process.
Oral lesions of histoplasmosis be present as:
1. Nodular lesions which may undergo central necrosis & lead to
2. Indurated ulcer which may be one or more
The ulcers: chronic, non-healing, single or multiple, indurated, painful
3. Verrucous or granular masses
4. Marked local tissue destruction with erosion into bone may occur any part of the oral
mucosa may be affected with such lesions.

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5. Pain associated with the lesions may prevent eating and cessation of oral hygiene leads to
severe halitosis
Histopathology:
Granulomatous reactive lesion including:
Micro-organism, macrophages and multinucleated giant cells.
Treatment: amphotericin + ketoconazole
❖ Viral infection
Structure of viruses:
1. Genome: the inner nucleic acid core, either DNA or RNA
2. Capsid: the protein coat, consists of identical sub units called capsomere
3. Envelop:surround many viruses, consists of lipoproteins
4. Virion: complete virus particle that consists of genome and capsid or genome, capsid and
envelop.
5. Inclusion bodies: virus induced masses seen in the nucleus or cytoplasm of infected cells
by light microscope. They are round and sharply demarcated area, strongly eosinophilic
with H& E stain.
Virus growth cycle:
1. Adsorption to specific receptor on the host cell
2. Penetration
- The virus penetrates the cell by a process similar to phagocytosis
- Uncoating(exposure of the viral nucleic acid) may occur during attachment or within
the host cells.
3. Replication
- Using the host cell ribosomes, energy and enzymes the virus replicates its own
components
4. Assembly
- The newly synthesized viral components are assembled to produce complete new
viruses
5. Release
- The host cell lyses releasing many virus particles
6. Invasion:
- The released virus particles infect another cell and the process begins a new cycle
Herpes simplex infection
There are 80 known herpesviruses, and eight of them areknown to cause infection in humans:
herpes simplex virus(HSV) 1 and 2, varicella-zoster virus, Cytomegalovirus,Epstein-Barr
virus, and human herpesvirus 6 (HHV6),HHV7&HHV8.

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Allherpesviruses contain a deoxyribonucleic acid (DNA) nucleusand can remain latent in host
neural cells, thereby evading thehost immune response. Humans are the only natural reservoir
of HSV infection,and spread occurs by direct intimate contact with lesions orsecretions from
an asymptomatic carrier.Latency, a characteristic of all herpesviruses, occurs whenthe virus is
transported from mucosal or cutaneous nerve endingsby neurons to ganglia where the HSV
viral genomeremains present in a non-replicating state. During the latentphase, herpes DNA is
detectable, but viral proteins are not produced. Reactivation of the latent virus occurs when
HSVswitches to a replicative state; this can occur as a result of anumber of factors including
peripheral tissue injury fromtrauma or sunburn, fever, or immunosuppression. There are two
types of herpes simplex virus:
HSV1
(A) Oral infection
1. Primary herpetic gingivostomatitis
2. Recurrent intraoral herpes
3. Recurrent herpes labialis
(B) Dermatitis above the waist
(C) Pharyngeal infection
(D) Meningoencephalitis
HSV2
(A) Genital infection
(B) Dermatitis below waist
(C) Infection in new born

o Primary Herpes Simplex Virus Infections (Acute herpetic gingivostomatitis)

Primary HSV infectionoccurs in patients who do not have immunity resulting fromprevious
contact with the virus. HSV is contracted after intimatecontact with an individual who has active
HSV primaryor recurrent lesions.Primary HSV may also be spread byasymptomatic shedders
with HSV present in salivary secretions.The majority of oral HSV infections is caused by
HSV1,but primary oral HSV2 infections may also occur chiefly as result of oral-genital contact.
Infection of the fingers (herpeticwhitlows) of health professionals may occur during treatmentof
infected patients. Dentists may experience primarylesions of the fingers from contact with
lesions of the mouthor saliva of patients who are asymptomatic carriers of HSV.
Clinical manifestation:
The patient usually presents to the clinician with full-blownoral and systemic disease, but a
history of the mode of onsetis helpful in differentiating lesions of primary HSV infectionfrom
other acute multiple lesions of the oral mucosa. Theincubation period is most commonly 5 to 7
days but mayrange from 2 to 12 days.

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Age:
Is more common in infant and children (1-10 years) with the highest peak between 2-3years.
Uncommon before 6 months because of maternal antibodies (IgG) that can cross the placental
barrier.
Not infrequent in adults but the manifestations are less typical and of shorter duration.

Features:
1. History of generalized prodromal symptoms that precede the local lesions by1 or 2
days.This information is helpful in differentiating thisviral infection from allergic
stomatitis or erythema multiforme,in which local lesions and systemic symptoms
appeartogether.These generalized symptoms include fever, headache, malaise, nausea,
vomiting, anorexia, arthralgia and cervical lymphadenopathy.
2. Generalized acute marginal gingivitis, 1-2 days the gingiva is intensely inflamed and
edematous, it is important diagnostic criteria.
3. Vesiculobullous lesions, small vesicles appear on the oral mucosa; these arethin-walled
vesicles surrounded by an inflammatory base. The vesicles quickly rupture, leaving
shallowround discrete ulcers. The lesions occur on all portions of themucosa. As the
disease progresses, several lesions may coalesce,forming larger irregular lesions.
Circumoral lesions, small multiple vesicles tend to occur in clusters on the vermillion
border of the lips as well as the circumoral skin. The vesicle may collapse or rupture,
ulcerate and covered by crust of purulent exudates due to secondary infection. In few cases
there are no intra-oral lesions and the lesions are confined to the lip and circumoral skin.
Ulcer: painful, superficial, round, small, surround by inflammatory hallow and covered by
a greyish membrane.
4. Excessive salivation: saliva contains large amounts of virus which can be detected up to
one month after onset of disease, and that can infect the skin around lips or eye and vagina
by patient’s hand.
Fact:
a. Self-limiting and resolves within 10-14 days
b. Shorter duration in adults
c. Sever in new born, immunocompromised patients.
Diagnosis:
1. Case history:
- History of prodromal features
- Positive history of contact with patient with primary or recurrent herpes

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- Negative history of previous recurrent heroes.

2. Clinical examination
- Inflammation of gingiva
- Multiple small shallow ulcers on keratinized and non-keratinized mucosa
- Lymphadenopathy: submandibular and upper deep cervical
3. Special investigation
Rarely is performed except in patients with less obvious clinical manifestation.
The investigation include:
a. Cytology: from un ruptured vesicles to demonstrate multinucleated giant cells and
ballooning degeneration of the nucleus using Giemsa or Wright stain.
Cytology smear to demonstrate the virus using fluorescent HSV antibody. It is more
sensitive (83%) compared with routine cytological smear (54%)
b. HSV isolation in tissue culture e.g. rabbit’s kidney
c. Antibody titer:
No antibody at the onset could be demonstrated in serum
Antibody begin to appear by 7-day reaching maximum value by 3 weeks (4 folds rise
during convalescence)
Treatment:
❖ Mild cases:
Since primary herpes is self-limiting disease, mild lesions can be managed with supportive
treatment only that includes:
- Bed rest
- A soft balanced diet with drinking to prevent dehydration
- Analgesic and antipyretic e.g. paracetamol
- Local anesthesia e.g. Tantumverde (benzydamine HCL) mouth bath
- Lidocaine 5% ointment, may be useful, although their duration of action is short
- Antiseptic mouth rinse e.g, 0.2 % chlorohexidine
❖ Severe oral involvement
Antiviral drugs should be prescribed as:
1. Rifampicin (it is antibiotic and have antiviral action)
Indication: severe primary herpetic gingivostomatitis in normal host
Doses: 10mg/ kg t.d.s. orally for 5 days
Or
- As mouth rinse then swallowed in adults
- By dropper in infants and young children
Advantage:
- Topical and systemic action of the drug
- Antibacterial and antiviral properties
2. Acyclovir (Zovirux)

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Indications:
- Disseminated disease in infants or atopic individuals
- Severe oral involvement in immune-compromised patients
- Severe oral involvement in healthy individuals
Doses:
Healthy patients > 12 years 200mg 5 times/day for 5 days
< 12 years 100 mg 5 times/day for 5 days
Immune-compromised patients 400 mg 5 times/day till healing
N.B. treatment of primary infection should be given within 3 days of the onset of symptoms but
not after that, because acyclovir may elicit resistant HSV without any clinical benefits.
o Recurrent herpetic lesions

Recurrent herpes infection of the mouth (recurrent herpeslabialis(Common cold sore)& recurrent
intraoral herpes simplex infectionoccurs in patients who have experienced a previous herpes
simplex infection and who have serum-antibody protectionagainst another exogenous primary
infection.
Recurrent herpes is not a re-infection but a reactivation of virusthat remains latent in nerve tissue
between episodes in a non-replicatingstate. Recurrent herpes may be activated by traumato the
lips, fever, sunburn, immunosuppression, and menstruation.The virus travels down the nerve
trunk to infectepithelial cells, spreading from cell to cell to cause a lesion.
Clinical features of recurrent herpes labialis
Prodromal symptoms of tingling, burning, or pain in the site in which lesions willappear.This is
accompanied by erythema, edema at the site of the lesion. Within a matter of hours, multiple or
cluster of vesicles appear.
Each vesicle is 1 to 3 mm in diameter, with the size of thecluster ranging from 1 to 2 cm
surrounding by erythema on vermillion border of the lips, especially on mucocutaneous junction.
These vesicles become ruptures and coalesce to form ulcers and covered by crust. The lesions heal
without scarring in 1 to 2weeks and rarely become secondarily infected.
The number of recurrences is variable and ranges from one per year to as many as one per month.
Therecurrence rate appears to decline with age and occur on previous site or near it.
Clinical features of recurrent intraoral herpes simplex
Are similar inappearance to RHL lesions, but the vesicles break rapidly toform ulcers. The
lesions are typically a cluster of small vesiclesor ulcers, 1 to 2 mm in diameter, clustered on a
small portionof the heavily keratinized mucosa of the gingiva, palate, andalveolar ridges.
Note: In contrast, lesions ofRAS tend to be larger, to spread over a larger area of mucosa,

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and to have a predilection for the less heavily keratinized buccalmucosa, labial mucosa, or floor
of the mouth.
Treatment
1. Sun block, or sun screen in case RHL or avoid exposure to sunlight, if it is the
predisposing factor.
2. Acyclovir ointment in case RHL, 5 times daily for 5 days should be started within 24
hours after the lesion onset, before the vesicles appear.
3. 2% tetracycline mouth bath after meals and before bed time.

• Chronic (aggressive) HSV infection

It is a severe recurrent form of herpes simplex infection type 1 & 2 that occurs in immune
suppressed patients.
Clinical features:
Intra-oral vesicles that ruptures to form ulcers. Ulcers features: crateriform in shape, well
defined raised borders, floor covered by grayish white pseudomembrane, large, deep and
painful.
Circumoral vesiclesbecome necrosis and crusted.
Fate: the lesion continues to enlarge to considerable large size unless treated with antiviral
drugs.
Treatments:
Acyclovir 400mg 5 times/ day until healing occurs.
• Varicella-Zoster Infections
Primary varicella-zoster virus (VZV) infections in seronegative individuals are known as
varicella orchickenpox, secondary or reactivated disease is known as herpes zoster or shingles.
Structurally, microscopically and the ability of the virus to remain quiescent insensory ganglia
(dorsal root ganglia of spinal nerves or extra-medullary ganglia of cranial nerves) for indefinite
periods after a primary infectionVZV is very similar to HSV.A number of signs and symptoms,
however, appear to be unique to each infection.
Clinical features
Chicken pox
Prodrome:Fever, chills, malaise,and headache may accompany a pruritic rash that involves
primarily the trunk and head and neck.

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Skin: Vesicles rapidly developinto on an erythematous base, then quickly develops into
pustular and eventually ulcerates. Successive crops of rashes continue to appear for 3-6 days
due to repeated waves of viremia. The lesion heals without scar formation unless secondary
infected by bacteria.
Oral: Multipleshallow ulcers that are preceded by vesicles.oral lesions do not present any
symptomatic, diagnostic, or management problem.
Note:Complications, including pneumonitis, encephalitis, and inflammation of other
organs,may occur in a very small percentage of cases. If varicella is acquired during
pregnancy, fetalabnormalities may occur.

Herpes Zoster (HZ)

Thenerves most commonly affected with HZ are C3, T5, L1, L2,and the first division of the
trigeminal nerve.
Prodromal period of 2 to 4 days,whenshooting pain, paresthesia, burning, and tenderness
appearalong the course of the affected nerve.
Skin:Unilateral vesicles on anerythematous base then appear in clusters, chiefly along
thecourse of the nerve, giving the characteristic clinical picture ofsingle dermatome
involvement but after few days it become pustules than rupture andturn to crust in 1 week.
Healing takes place within 3-4 weeks by scar formation, these scars are diagnostic in case of
post herpetic neuralgia.
Oral:Herpes zoster involves one of the divisions ofthe trigeminal nerve in 18 to 20% of cases,
but the ophthalmicbranch is affected several times more frequently than are thesecond or third
divisions.Facial and intraoral lesions arecharacteristic of HZ involving the second and third
divisionsof the trigeminal nerve.Each individual oral lesion of HZ resembles lesions seenin
herpes simplex infections. The diagnosis is based on a historyof pain and the unilateral nature
and segmental distributionof the lesions.
Healing may be associated by scarring. Bilateral lesions may occur due to viremia.
Diagnosis:
a. Case history
b. Clinical examination:
Unilateral, painful, dermatomic distribution
c. Special investigation: as HSV infection
Treatment:
Basic line of treatment includes:

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1. Antiviral therapy: acyclovir, famcyclovir&valacyclovir

2. Pain control: NSAIDs alone or combination codeine or in severe case pethidine some time
low intensity laser therapy which accelerate healing because it improves cellular repair and
stimulation of the immune, lymphatic and vascular systems.
• Mild clinical manifestation:
- Sedation and potent analgesic
Extreme care to avoid secondary infection by: 0.2% chlorhexidine mouthwash
- 5% acyclovir ointment for skin and eye lesion
- Topical capsaicin
N.B. topical anesthesia are not effective since the pain arise from the sensory nerve.
• Severe clinical manifestation:
- Acyclovir 800 mg tablets 5 times per day for 7-10 days.
N.B. acyclovir and prednisone 40- 60 mg/ day decreasing over 3 weeks hoping to prevent post
herpetic neuralgia.
Ramsay Hunt syndrome, in which facial paralysis is accompanied by vesicles of the ipsilateral
externalear, tinnitus, deafness, vertigo and vesicles of oral mucosa.
Complication of herpes zoster
Common in immunocompromised and elderly patients
1. Post herpetic neuralgia:
Pain remaining for over a month after the mucocutaneous lesions have healed.The overall
incidence of postherpetic neuralgia is 12 to 14%, but the risk increases significantly after
the age of 60 years, most likely due to the decline in cell-mediated immunity.
2. Generalized herpes zoster; involving internal organs leading to pneumonia,
meningoencephalitis and hepatitis.
3. Motor paralysis
4. Secondary infection
5. Blindness when ophthalmic division is involved.

o Coxsackie virus infections

Coxsackie virus is RNA enterovirus, separated into groups A and B. There are about 24 types of
Coxsackie A & 6 types of B. Type A virus is important to the dentist because it can induce three
varieties of infection in the mouth and oropharyngeal region:
i. Herpangina
ii. Hand, foot and mouth disease
iii. Acute lymphonodular pharyngitis

o Herpangina

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Herpangina is an acute viral infection caused by Coxsackie type A virus (A4 has been shown to
cause a majority ofcases, types A1-10, A16,A22, and possibly others)Because many
antigenicstrains of Coxsackievirus exist, herpangina may be seen morethan once in the same
patient.
Clinical Features
It is usually endemic, with outbreaks occurring typically in summer or early autumn.
Age:It is morecommon in children (3-10 ys) than in adults.
Prodromal: malaise, fever, dysphagia, andsore throat after a short incubation period.
Orally:Lesions start as punctate macules,which quickly evolve into papules and vesicles
involvingthe posterior pharynx, tonsils, faucial pillars, and soft palate.Lesions are found less
frequently on the buccal mucosa,tongue, and hard palate.
Within 24 to 48 hours,the vesicles rupture, forming small 1 to 2 mm ulcers. The diseaseis usually
mild and heals without treatment in 1 week.
Herpangina may be clinically distinguished from primaryHSV infection by several criteria:
1. Herpangina occurs in epidemics; HSV infections donot.
2. Herpangina tends to be milder than HSV infection.
3. Lesions of herpangina occur on the pharynx and posteriorportions of the oral mucosa, whereas
HSV primarilyaffects the anterior portion of the mouth.
4. Herpangina does not cause a generalized acute gingivitislike that associated with primary HSV
infection.
5. Lesions of herpangina tend to be smaller than those ofHSV.
o Hand, foot and mouth disease
It is caused by infection with Coxsackievirus A16 in a majority of cases.
Clinical features
Age:8 months to4 years of age.
low-grade fever, non-pruritic macules, papules, and vesicles, particularly on the extensorsurfaces
of the hands and feet.
Orally:oral vesicles and ulcers are moreextensive than are those described for herpangina, and
lesionsof the hard palate, tongue, and buccal mucosa are common.
Treatment is supportive.
o Acute lymphonodular pharyngitis

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This is a variant of herpangina caused by Coxsackievirus A10.The distribution of the lesions is

the same as in herpangina,but yellow-white nodules appear that do not progress to vesiclesor
ulcers. The disease is self-limiting, and only supportivecare is indicated.

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