Describes the features, pathogenesis, diseases caused by herpes simplex virus and treatment modalities followed by dental implications

1. HERPES SIMPLEX
INFECTION IN ORAL
CAVITY
HRISHITA

2. INTRODUCTION
■ Herpes simplex virus 1 and 2 belong to a family of viruses called
Herpesviridae
Herpes simplex 1 Herpes simplex 2

3. ■ Infections above the waist are caused by Herpes
simplex1
■ Infections below the waist are caused by Herpes
simplex 2
■ Though in recent times, changes in sexual practices
can lead to cultivation of HSV2 from oral lesions and
vice versa

4. P
A
T
H
O
G
E
N
E
S
I
S
Initial infection occurs by inoculation of the mucosa, skin or eyes with infected secretions
Virus travels along the sensory nerve axons
Neuronal latency - Establishes chronic, latent infection in sensory ganglion
(eg. Trigeminal nerve)
Or
Extra neuronal latency-HSV remains latent in sites other than neurons (eg. Epithelium)
Reactivation of HSV at latent sites and centripetal movement to mucosa or skin occurs
Cytopathic effect on epithelial cells
Recurrent or Recrudescent HSV
AFTER A PERIOD OF LATENCY

5. TYPE OF
HUMAN
HERPES
VIRUS
PRIMARY INFECTION
(Subclinical)
RECRUDESCENT LESSION IN
HEALTHY HOSTS
RECRUDESCENTT LESIONS IN
IMMUNOCOMPROMISED HOSTS
HSV 1 • Gingivostomatitis
• Keratoconjunctivitis
• Herpetic whitlow
• Herpetic gladiatorum
• Herpes encephalitis
• Esophagitis
• Pneumonia
• Herpes labialis (cold sores,
fever blisters)
• Intraoral ulcers
• Keratoconjunctivitis
• Ulcers at any site; usually large
and persistent
• Disseminated infection
HSV 2 • Genital lesions
• Gingivostomatitis
• Keratoconjunctivitis
• Neonatal infections
• Aseptic meningitis
• Genital and skin lesions
• Gingivostomatitis
• Ulcers at any site; usually large
and persistent
• Disseminated infection
INFECTIONS CAUSED BY HERPES SIMPLEXVIRUS

6. ORAL
MANIFESTATION
S OF HERPES
SIMPLEX

7. HERPETIC GEOMETRICGLOSSITIS
• Rare cause of fissuring of tongue
• Immunocompromised hosts
• Presents with acute onset of pain
• Deep longitudinal, crossed or branched linear
grooves with smaller lateral fissures
• Treated with systemic antiviral drugs

8. PRIMARY GINGIVOSTOMATITIS
■ Children, teenagers and young adults
■ 1- 3 day viral prodrome
■ Fever, loss of appetite, malaise, myalgia,
headache and nausea
■ Oral pain causes poor oral intake thus
patients may need hospitalization
■ Self limiting; resolves in 10-14 days
■ In children, may be misdiagnosed as
TEETHING
■ Marginal gingiva- rule of thumb
■ In adults- pharyngeal tonsillitis

9. ORAL FINDINGS
■ Clusters of vesicles on keratinized mucosa and non
keratinized mucosa
■ Vesicles break down to form ulcers with scalloped
borders and marked surrounding erythema
■ Yellowish exudate
■ Erythematous gingiva
■ Extremely painful mouth
■ Pharyngitis causes difficulty in swallowing

10. RECRUDESCENT ORAL HSV
INFECTION
■ The term RECRUDESCENT is used for ulcerations caused by reactivated HSV VIRUS
■ Transmission of virus is by shedding through bodily secretions- this is usually
asymptomatic
■ Ulcerations may occur
■ TRIGGER FACTORS- UV radiation, stress, trauma, menstruation

11. RECRUDESCENT ORAL HSV INFECTIONS
Recrudescent
intraoral herpes
infection (RIH)
Immunocompromised Immunocompetent
Recurrent
herpes labialis

12. RECURRENT HERPES LABIALIS
■ Seen in the vermilion border of lips
■ PRODROMAL FEATURES- Tingling, itching or burning
■ Appearance of papules, vesicles, ulcers and crustings
■ Spontaneous resolution of the lesions
■ Pain is seen only for the first 2 days
■ Some patients don't experience a prodrome
■ These patients have lesions that have experienced from extraneural
latent HSV (epithelium)
■ Extraneural latent HSV is less responsive to Topical therapy

14. RECRUDESCENT INTRAORAL HSV
(RIH)
IN IMMUNOCOMPETENT HOSTS
■ Keratinized mucosa (palate, dorsum of tongue
and attached gingiva)
■ Single or clustered painful ulcers with a bright
red erythematous border

15. RECRUDESCENT INTRAORAL
HERPES IN IMMUNOCOMPROMISED
■ Intra oral site (keratinized and non
keratinized sites)
■ Forms large ulcers
■ Appear slightly depressed with raised
borders
■ Vesicles and satellite ulcers at the edges of
the main ulcer
■ May last for several weeks or months if
undiagnosed and untreated

16. ■ In untreated patients, RIH infection may disseminate to
other sites and cause severe infections- most commonly
seen hematopoietic stem cell transplantation patients

17. DIFFERENTIAL DIAGNOSIS

18. COXSACKIE VIRUS INFECTION (HAND-
FOOT-MOUTH DISEASE)
PRIMARY HERPETIC GINGIVOSTOMATITIS
Ulcers are not clustered Clustered ulcers
Generalized gingival inflammation
absent
Generalized gingival inflammation seen
1)

19. HERPANGINA PRIMARY GINGIVOSTOMATIS
Occur in epidemics Does not occur in epidemics
Pharynx and posterior mucosa Anterior mucosa
Generalized acute gingivitis absent Generalized acute gingivitis present
Milder Severe
Smaller lesions Larger lesions
2)

20. NECROTIZING ULCERATIVE GINGIVITIS RIH INFECTION IN IMMUNOCOMPETENT
Widespread and diffuse lesions Localized lesions
Cultures positive for fusobacterium and
spirochetes
Cultures positive for HSV
Predisposing factors present like diabetes Precipitating cause such as dental
treatment
3)

21. TRAUMATIC ULCERS RIH INFECTION
Signs of trauma No such signs will be visible in the cavity
No microorganism culturable Culture positive for HSV
4)

22. APHTHOUS ULCERS RIH INFECTION
Non Keratinised mucosa Keratinised mucosa
Vesicles or satellite ulcers absent Vesicles or satellite ulcers present at the
edges of main ulcer
Culture negative for HSV Culture positive for HSV
5)

23. LABORATORY DIAGNOSIS
 HSV isolation by cell culture is Gold Standard Test
ADVANTAGES-
1) high sensitivity and specificity
2) allows for amplification of virions
3) subtyping
4) grows readily in tissue culture
5) testing for sensitivity to antiviral drugs
DISADVANTAGES-
1) specialized equipment
2) expensive
3) need for special transport
4) may show false positive results

24. Tzank Staining
• HSV can be identified from base of lesions
• WRIGHT OR GIESMA (TZANK PREPARATION)
• PAPNICOLAOU STAIN
• Characteristic multinucleated giant cell and ballooning
degeneration seen
• Intranuclear Inclusions seen (LIPSCHUTZ BODIES)
• However doesn't distinguish between HSV and VZV

25.  Polymerase Chain Reaction from swabs detects HSV Antigen
3-4 times more than culture
 Direct Fluorescent antigen testing- more accurate than cytology
 Serology

26. MANAGEMENT
3 Goals in management of HSV infections-
1)Pain control
2)Supportive care
3)Definitive treatment

27. A) PAIN CONTROL
DRUG DOSAGE FREQUENCY INSTRUCTIONS
2% viscous lidocaine 5ml 4-5 times a day Swish and spit
Liquid diphenhydramine 5ml 4-5 times a day Swish and spit
Combination of viscous
lidocaine,
diphenhydramine, covering
agent (kaopectate or
maalox)
1:1:1 ratio - -
Benzydamine (Tatum
mouthwash)
- - -
Systemic analgesia - - -

28. B) SUPPORTIVE CARE
Hydration
Ice chips or popsicles
Soft bland diet
Antipyretics and analgesics as required

29. C) DEFINITETREATMENT
DRUG DOSAGE FREQUENCY APPLICATION
PRIMARY HSV INFECTION
Acyclovir 15mg/kg 5 times a day Systemic
Valacyclovir - -
Famciclovir - -
RECURRENT HERPES LABIALIS
Acyclovir cream 5% 5-8 times a day Topical
Penciclovir cream 1% 5-8 times a day
Docosanol cream 10% 5-8 times a day
Valacyclovir 2 g Every 12 hrs for 1 day Systemic
Famciclovir 1500mg Single dose

30. DRUG DOSAGE FREQUENCY APPLICATION
RECURRENT INTRAORAL HERPES
Valacyclovir 500-1000mg 3 times a day Systemic
Famciclovir 400-800 mg 7-10 days
HSV SEROPOSITIVE UNDERGOING HAEMATOPOIETIC CELLTRANSPLANTATION
Acyclovir 400mg 3 times a day Systemic
Valciclovir 500mg 2 times a day
Foscarnet or cidofovir is given in acyclovir resistant HSV

31. INFECTION CONTROL
■ Usage of GLOVES reduces spread Herpes infection
■ Postpone the treatment in case lesions are active
and oozing
■ Emergency application of RUBBER DAMS reduces
virus transmission to other sites

32. HERPETICWHITLOW
• Intense painful infection of the fingers or toes
• Children, adults and health care workers
• Terminal phalanx of index and thumb fingers
• Prodromal symptoms of burning or tingling
and pruritus
• Multiple tiny vesicles which are extremely
tender
• Surrounding area appears edematous and
erythematous
• Lesion ruptures to form shallow ulcers
• Heal in 10 days time

33. CONCLUSION
■ Herpes infection is a common infection seen in dental clinics
■ So as future clinicians, we must aim to
– Identify the lesions with proper history and clinical examination
– Provide the patient with best treatment
– Measures to prevent further spread of the infection

34. BIBLIOGRAPHY
■ BURKET’S ORAL MEDICINE 12TH EDITION
■ ONGOLE
■ SHAFER’S 8TH EDITION