1. ORAL CAVITY
Ulcerative &
Inflammatory
Lesions
Lecture 1 New
By Dr Mohammad Manzoor Mashwani

2. Ulcerative & Inflammatory
Lesions of
Oral Cavity
• Aphthous Ulcers
• Herpesvirus Infection
• Oral Candidiasis
• AIDS & Kaposi Sarcoma

3. CACKER SORES
APHTOUS
ULCERS
APHTHAE
RUCURRENT APHTHOUS STOMATITIS

4. DEFINITION
• It is the most common disease
characterized by the development of
painful, recurring ,solitary or multiple
ulcerations of the oral mucosa.

5. Synonyms
Canker
Sores
Recurrent
Aphthous
Stomatitis
Aphthae

6. APTOUS/ CANKER

7. • Age. More common in the first 2
decades of life
• Triggers: stress, fever, ingestion
of certain foods and activation of
inflammatory bowel disease.

8. Causes

9. Gross Morphology
• The lesions appear singly or in
groups
• on the nonkeratinized oral
mucosa, particularly the soft
palate, bucolabial mucosa, floor
of the mouth, and lateral borders
of the tongue.
Nonkeratinized squamous epithelium covers the soft palate,
inner lips, inner cheeks, and the floor of the mouth, and ventral
surface of the tongue. Keratinized squamous epithelium is
present in the attached gingiva and hard palate as well as areas
of the dorsal surface of the tongue.

10. GROSS Morphology
•
•
•
•
•
Small (< 5mm),
Shallow Ulcers
Rounded, superficial erosions,
Covered with gray-white exudate,
Having an erythematous rim.

13. Treatment
• The canker sores are self-limited
and usually resolved within a few
weeks, but they may
recur
in the same or different location
in the oral cavity.

14. HERPESVIRUS
INFECTION
/Crawl )

15. Herpesvirus Infection
• ‘Extremely common infection caused by
HSV1
• Transmitted from person to person by
kissing.
• By middle life over ¾ of the population
have been infected.

16. • They occur most often on
the lips or about the nasal
orfices and are well known
as cold sores or fever
blisters. They soon rupture,
leaving shallow, painful
ulcers that heal within a
few weeks, but
recurrences are common.

17. Pathogenesis
• In most adults the primary
infection is asymptomatic, but
the virus persists in a
dormant state within
ganglia about the mouth
(trigeminal ganglia).

18. • With reactivation of the virus
(which may be caused by
fever, sun or cold
exposure, respiratory tract
infection, trauma), solitary or
vesicles
multiple small
containing clear fluid appear.

19. Pathogenesis
Entry by skin or mucous membranes
viral multiplication
sensory nerve
lysis of cells
root ganglia
vesicles
ulcers
latency
REACTIVATION
COLD
FEVER
SURGERY
UNKNOWN

20. Morphology
• The vesicles begin as intraepithelial focus of
intercellular and intracellular EDEMA.
• The infected cells become BALLONED and develop
intranuclear acidophilic viral INCLUSIONS.
Sometimes adjacent cells fuse to form GIANT CELLS
known as
MULTINUCLEATED
POLYKARYONS.

21. • Necrosis of the infected cells and the
focal collections of edema fluid
account for the INTRAEPITHELIAL VESICLES
detected clinically.
• Identification of the inclusion-bearing cells or
polykaryons in smears of blisters fluid
constitutes the diagnostic Tzanck test for
HSV infection.

22. Herpetic Gingivostomatitis
• In 10-20% of those with this conditionparticularly in the immunocompromised– a
more virulent disseminated eruption
develops, producing multiple vesicles
throughout the oral cavity, including the
gingiva and pharynx (herpetic
gingivostomatitis), and
lymphadenopathy.

25. In particularly severe
cases, viremia may seed
the brain (causing
encephalitis) or produce
dissiminated visceral
lesions.

26. HSV type 1 may localize in conjuntivae
(Keratoconjunctivitis) and the
esophagus when a NG tube is
introduced though an infected oral
cavity.
As a result of changes in sexual
practices, genital herpes produced by
HSV type 2 (the agent of herpes
genitalis) is increasingly seen in the
oral cavity, producing vesicles in the
mouth.

27. Oral Candidiasis
• Candida albicans is a normal
inhabitant of the oral cavity found
in 30-40% of the population; it
causes disease only when there is
impairment of the
usual protective
mechanism.
some

28. • Pseudomembranous candidiasis
(thrush, moniliasis) is the most
common fungal infection of the
oral cavity and is particularly
common among persons rendered
vulnerable by diabetes mellitus,
immunodeficiency, or debilitating
illnesses such as disseminated
cancer. Persons with the acquired
immunodeficiency (AIDS) are at
particular risk.

29. Morphology
An adherent white, curd like,
circumscribed PLAQUE anywhere
within the oral cavity.
The pseudomembrane can be
scraped off to reveal an
underlying granular erythematous
inflammatory base.

30. Microscopy
• The pseudomembrane is composed of a
myriad of fungal organisms
superficially attached to the underlying
mucosa.
• In milder infections there is minimal
ulceration, but
• in severe cases the ENTIRE MUCOSA may
be denuded.

31. • Dissiminated candidiasis is a life
threatening infection that must be treated
aggressively.

32. AIDS & Kaposi Sarcoma
• AIDS is often associated with lesions in
the oral cavity.
• They may take the form of candidiasis,
herpetic vesicles, or some others microbial
infection (producing gingivitis or glossitis).

33. AIDS & Kaposi Sarcoma
• Hairy leukoplakia is an uncommon lesion seen
virtually only in persons infected with HIV.
• It consists of white confluent patches, anywhere
on the oral mucosa, that have a “hairy” or
corrugated surface resulting from marked
epithelial thickening.It is caused by Epstein-Barr
virus infection of epithelial cells. Occasionally, the
development of hairy leukoplakia calls attention to
the exitence of the underlying HIV infection.

34. AIDS & Kaposi Sarcoma
• More than 50% of individuals with Kaposi
sarcoma develop intraoral purpuric
discolorations or violaceous, raised, nodular
masses; sometimes this involvement
constitutes the presenting manifestation.
Kaposi sarcoma is a tumor caused
by human herpesvirus 8.