Etiology, Clinical features, Histopathological features, Differential diagnosis , Treatment of Primary Herpetic gingivostomatitis

1. Presented by
OLGA MCFRANCIS
FINAL YEAR BDS PART 1
Acute Gingival
Infections- Herpetic
Gingivostomatitis
DEPARTMENT OF PERIODONTICS ,
GOVT DENTAL COLLEGE, TRIVANDRUM

2. CONTENTS
• Introduction
• Classification
• Primary Herpetic
Gingivostomatitis
• Mode of Transmission
• Pathogenesis
• General Features
• Clinical Features
• Histopathology
• Diagnosis
• Differential Diagnosis
• Conclusion
• Recent Studies
• Previous year Questions
• Bibliography
• Treatment

3. INTRODUCTION
Acute gingival infections often present with
painful intraoral or perioral lesions. Patients
presenting with acute infections require
urgent treatment to relieve symptoms and to
resolve the infection.This seminar reviews the
presenting history, signs, symptoms, clinical
features, diagnosis, treatment,etc of primary
herpetic gingivostomatitis.

4. Classification of Acute
Gingival Lesions

5. Primary Herpetic Gingivostomatitis
• Herpes simplex, an acute infectious disease, is probably the most
common viral disease affecting man, with the exception of viral
respiratory infections.
• HSV is composed of double-stranded DNA, protein capsid,
tegument and lipid envelope,which contain glycoproteins derived
from the nuclear membrane of host cells.
• There are two immunologically different types of HSV: type 1 and
type 2
• HSV-1 predominantly affects the face, lips, oral cavity and upper
body skin
• HSV-2 usually affects the genitals and skin of the lower half of the
body.

7. Mode of
transmission
• It can be due to droplet spread.
• There is no animal reservoir for
this virus.
• The incubation period appears
to range from 2 to 20 days, with
an average of 6 days before
development of lesions.

8. Pathogenesis
• The virus is attached to the cells at the inoculation site through
specific receptors .
• It replicates too many virions to the maximum number, and
discharges to neighbouring cells.
• Subsequently, it affects adjacent cells, spreads to distant
sensory nerve endings and autonomic axons, further to
adjacent related ganglia,and remains latent there.
• The lymph node is involved through viral proteins by mobile
dendritic cells and begins its primary immune response.

9. Pathogenesis

10. General Features
• Mostly in infants and children less than 6 years
old.
• Seen in adolescents and adults also.
• Male : Female equal
• Mostly Primary Infections are asymptomatic.
• As part of the primary infection, the virus ascends
through the sensory and autonomic nerves where
it persists as latent HSV inneuronal ganglia that
innervate the site.

11. • In approximately one-third of the
world’s population, secondary
manifestations result from various
stimuli, such as sunlight, trauma,
fever, and stress.
• These secondary manifestations
include herpes labialis,herpetic
stomatitis,herpes genitalis, ocular
herpes, and herpetic encephalitis.

12. • Secondary herpetic stomatitis can
occur on the palate, on the gingiva or
on the mucosa as a result of dental
treatment that traumatizes or
stimulates the latent virus in the ganglia
that innervate the area.
• It may be present as pain away from the
site of treatment 2–4 days later.

13. • Diffuse,erythematous, shiny involvement of the
gingiva and the adjacent oral mucosa, with
varying degrees of edema and gingival
bleeding.
• During its initial stage, it is characterized by the
presence of discrete, spherical gray vesicles,
which may occur on the gingiva, the labial and
buccal mucosae, the soft palate, the pharynx,
the sublingual mucosa, and the tongue
Clinical Features
Oral signs

14. • After 24 h, vesicles rupture and form painful small
ulcers with red, elevated, halo-like margins and
depressed yellowish or grayish-white central
portions.
• These occur either in widely separated areas or in
clusters where confluence occurs.
• Course of the disease is limited to 7–10 days.
• The diffuse gingival erythema and edema that
appear early during the course of the disease persist
for several days after the ulcerative lesions have
healed.
• Scarring does not occur in the areas of healed
ulcerations.

16. Oral Symptoms
• It is accompanied by generalized “soreness” of
the oral cavity, which interferes with eating,
drinking, and oral hygiene.
• Ruptured vesicles are the focal sites of pain.
• They are sensitive to touch, thermal changes,
foods such as condiments and fruit juices, and
the action of coarse foods.
• In infants, it is marked by irritability and refusal
to take food.

17. Extraoral and systemic signs and
symptoms
• Cervical adenitis
• Fever as high as 101–105°F (38–40.6°C)
• Generalized malaise

18. • Primary herpetic gingivostomatitis is the
result of an acute infection by HSV, and it
has an acute onset.
Histor
y

19. • The herpetic vesicle is an intraepithelial blister filled with
fluid. The infected cells are swollen and have pale
eosinophilic cytoplasm and large vesicular nuclei,
described as 'ballooning degeneration', while others
characteristically contain intranuclear inclusions known as
Lipschutz bodies.
• These are eosinophilic, ovoid homogeneous structures
within the nucleus, which tend to displace the nucleolus
and nuclear chromatin peripherally.
• The displacement of chromatin often produces a peri-
inclusion halo.
Histopathology

20. Histopathology

21. Histopathology
• Cytoplasm of the infected cells forms giant
cells.
• The subjacent connective tissue is usually
infiltrated by inflammatory cells.
• When the vesicle ruptures, the surface of the
tissue is covered by exudates made up of
fibrin, polymorphonuclear leukocytes and
degenerated cells.
• The lesions heal by peripheral epithelial
proliferation.

22. • Diagnosed both clinically and by laboratory
procedures.
• Scrapings obtained from the base of the
lesions are stained with Wright's and Giemsa
stains.
• Pap stain shows balloon cells, multinucleated
giant cells and intranuclear inclusions.
• Although cytological procedures give a quick
result but it will not differentiate between HSV
and varicella zoster virus (VZV).
Diagnosis
Pap Smear

23. Diagnosis

24. Diagnosis
• HSV can be demonstrated in the
laboratory by the isolation of
virus in tissue culture or by DNA
in the scrapings from lesions.
• The most sensitive and accurate
method for diagnosing these
lesions is the PCR technique.

25. Differential
Diagnosis
• Necrotising Ulcerative Gingivitis
• Erythema Multiforme
• Steven - Johnson Syndrome
• Aphthous Stomatits ( canker
sores)

26. Difference between
NUG & PHG

27. Treatment
• Topical Lignocaine for pain relief.
• Acyclovir 15mg/kg 5 times daily for 5-7 days reduces
duration of disease, halts the progression of lesions and
reduces infectivity.

28. • According to Irish Journal of Medical Science( 1971) , an article on Adolescents
and Herpetic Gingivostomatitis: an Italian Overview published on 15 May 2021,
• In Italian adolescents, PHGS was diagnosed atleast 48 h after onset and an
antibiotic therapy was prescription in order to prevent secondary bacterial
infections.
• 15 patients had been treated with non alcoholic chlorhexidine rinses ( Group A)
• 29 patients with non alcoholic chlorhexidine rinses plus hyaluronic acid gel (
Group B),
• 30 patients with non alcoholic chlorhexidine rinses plus Mucosyte ( Group C).
• A significant improvement of the pain scoring and lesions severity was noted in
Group C .
• Among topical therapies , an association of Verbascoside and Sodium
Hyaluronhate seems to favor faster healing.
Recent Studies

29. • Acute Herpetic Gingivostomatitis - it's causes, clinical
presentation and treatment. (2+2+4) [January 2020]
• Primary Herpetic Gingivostomatitis [January 2023,
2016 Scheme]
• Acute Herpetic Gingivostomatitis (AHGS) [July 2022]
Previous year questions

30. Bibliography
• Newman and Carranza's CLINICAL
PERIODONTOLOGY - Third South Asian Edition
• Essentials of CLINICAL PERIODONTOLOGY AND
PERIODONTICS by Shantipriya Reddy - 6th Edition
• Shafer's Textbook of ORAL PATHOLOGY -Ninth
Edition