3. Primary HSV Infections : childhood disease, generalized acute
marginal gingivitis, anterior portion of the mouth
Coxsackievirus Infections (Herpangina): childhood disease,
epidemics, posterior portions of the oral mucosa
Coxsackievirus Infections (Hand-foot-mouth disease): nonpruritic
lesions on the extensor surfaces of the hands and feet, the oral lesions
are more extensive
Varicella-Zoster Virus Infection (chickenpox, varicella): childhood
disease, generalized pruritic eruption of maculopapular skin lesions
that rapidly develop into vesicles
Varicella-Zoster Virus Infection (shingles, herpes zoster): with age
or immunosuppression, prodromal period (shooting pain,
paresthesia, burning, tenderness) along the course of the affected
nerve, clusters of unilateral vesicles along the course of the nerve,
postherpetic neuralgia
10. The most common triggers for episodes of EM are;
1- herpes simplex virus
2- drug reactions:
- NSAIDs: Oxycam, Diclofenac
- Anticonvulsants: Carbamazepine, Phenobarbital, Phenytoin
- Trimethoprim-sulfonamide combinations
- Allopurinol
- Penicillin
Many cases of EM continue to have no obvious detectable
cause.
Local lesions and systemic symptoms appear together
11. The pathognomonic skin lesion is the target or iris lesion,
which consists of a central bulla surrounded by bands of
erythema.
EM oral lesions are large, irregular, deep ulcers and often
bleed.
12. Mild cases of oral EM may be treated with supportive
measures only, including topical anesthetic mouthwashes and
a soft diet.
Moderate to severe oral EM may be treated with a short
course of systemic corticosteroids.
EM is classified as Stevens-Johnson syndrome when the
generalized vesicles and bullae involve the skin, mouth, eyes,
and genitals.
The most severe form of the disease is toxic epidermal
necrolysis, results in sloughing of skin and mucosa in large
sheets. Mortality, which occurs in 30-40% of patients, results
from secondary infection, fluid and electrolyte imbalance, or
involvement of the lung, liver, or kidneys.
13. Contact Allergic Stomatitis
• Contact allergy results from a delayed hypersensitivity
reaction
• The incidence of contact stomatitis is less common than
contact dermatitis for the following reasons:
1. Saliva dilutes potential antigens.
2. penetrating antigens are rapidly removed by vascular oral
mucosa before an allergic reaction can be established.
3. The oral mucosa has less keratin than does the skin,
decreasing the possibility of immune response.
14. Clinical findings:
Nonspecific lesions occur at the site of contact and include
a burning sensation accompanied by erythema, vesicles and
ulcers.
Lesions that appear lichenoid both clinically and
histologically
Another oral manifestation of contact allergy is plasma cell
gingivitis, which is characterized by generalized erythema and
edema of the attached gingiva
15. Oral Ulcers Secondary to Cancer Chemotherapy
Indirectly depress the bone marrow and immune response,
leading to bacterial, viral, or fungal infections of the oral
mucosa.
Direct effect on the replication and growth of oral epithelial
cells by interfering with nucleic acid and protein synthesis,
leading to thinning and ulceration of the oral mucosa.
16. Acute necrotizing ulcerative gingivitis
Endogenous oral infection that is characterized by painful
necrotic punchedout ulcerations, developing most commonly
on the interdental papillae and the marginal gingivae.
The constitutional symptoms are usually of minor significance
when compared with the severity of the oral lesions.
17. Classic ANUG in patients without an underlying medical
disorder is associated with three major factors:
1. Poor oral hygiene.
2. Smoking
3. Emotional stress
Systemic disorders associated with ANUG are diseases
affecting neutrophils (such as leukemia or aplastic anemia)
The gingivae should be débrided with both irrigation and
periodontal curettage. Careful home care instruction must be
given to the patient regarding rinsing and gentle brushing with
a soft brush. Metronidazole and penicillin are the drugs of
choice .
18. Recurring oral lesions
Recurrent Aphthous Stomatitis
Recurring ulcers confined to the oral mucosa in patients
with no other signs of disease
Heredity, immunologic disorders, hematologic
deficiencies, and allergic or psychological abnormalities have
all been implicated in cases of RAS.
19. prodromal burning erythema papule
ulcerates
The individual lesions are round, symmetric, shallow and
no tissue tags.
viral ulcers tissue tags
EM, pemphigus, pemphigoid irregular ulcers
20. Minor ulcers over 80% of RAS cases, less than 1 cm
in diameter, heal without scars
Major ulcers deep lesions, larger than 1 cm in diameter,
painful and interfere with speech and eating, last for months,
heal slowly and leave scars.
Herpetiform The least common variant of RAS, small
punctate ulcers scattered over large portions of the oral
mucosa.
21. Topical anesthetic agent or topical diclofenac, topical
steroid preparation, such as betamethasone or clobetasol,
topical tetracycline
In patients with major aphthae or severe cases of multiple
minor aphthae not responsive to topical therapy, use of
systemic therapy should be considered.
22. Behçet’s syndrome
Behçet’s syndrome is caused by;
- Immunocomplexes that lead to vasculitis
- Inflammation of epithelium caused by T lymphocytes.
There is a genetic component to the disease, with a strong
association with HLA-B51
23.
24.
25. Diagnostic criteria include;
recurrent oral ulceration at least three times in one year plus
two of the following:
1. Recurrent genital ulceration.
2. Eye lesions including uveitis or retinal vasculitis.
3. Skin lesions including erythema nodosum,
pseudofolliculitis, acneiform nodules.
4. A positive pathergy test; inflammatory reaction forming
within 24 hours of a needle puncture.
26. Recurrent Herpes Simplex Virus Infection
recurrent herpes
labialis
recurrent intraoral
herpes simplex infection
preceded by a prodromal period of tingling or
burning, edema at the site of the lesion, cluster of
small vesicles
similar in appearance to recurrent herpes labialis
lesions, clustered on a small portion of the heavily
keratinized mucosa (gingiva, palate, alveolar ridges)
27. Recurrent herpes is not a re-infection but a reactivation of
virus that remains latent in nerve tissue, the virus travels down
the nerve trunk to infect epithelial cells
Recurrent herpes may also be activated by trauma to the
lips, fever, sunburn, immunosuppression, emotional stress and
menstruation.
28. Chronic multiple oral lesions
Pemphigus vulgaris
binding of IgG autoantibodies
to desmosomes
separation of cells
[acantholysis]
destruction of desmosomescellular degeneration
and suprabasilar bulla
29. shallow irregular ulcers, the edges of the lesion continue to
extend peripherally over a period of weeks until they involve
large portions of the oral mucosa, desquamative gingivitis,
pressure to an apparently normal area results in the formation
of a new lesion [Nikolsky sign].
30. Patients with PV included in the differential diagnosis must
have a biopsy done for;
routine histology
direct
immunofluorescence
indirect
immunofluorescence
31.
32. Mucous membrane pemphigoid:
autoantibodies basement membrane subepithelial split
vesicle
• Erosions typically spread more slowly than pemphigus
lesions, more self-limiting, desquamative gingivitis
33. Patients with MMP included in the differential diagnosis must
have a biopsy done for
routine histology
direct
immunofluorescence
indirect
immunofluorescence
-ve
34. Erosive lichen planus
extensive degeneration of the basal layer of epithelium
causes a separation of the epithelium from the underlying
connective tissue.
The cause of lichen planus is unknown.
Where a causal or triggering agent is identified, this is
termed a lichenoid reaction rather than lichen planus. These
may include;
- Lichenoid drug eruptions: NSAIDs, hydrochlorothiazide,
penicillamine, angiotensin-converting enzyme inhibitors
- Lichenoid contact reactions: reactions to amalgam fillings
- Lichenoid reactions of graft-versus-host disease: due to bone
marrow transplantation.
35. A diagnosis of erosive lichen planus should be suspected
when erosive lesions are accompanied by typical lichenoid
white lesions.
Biopsy is necessary for definitive diagnosis. Biopsy of the
erosive lesions shows hydropic degeneration, [one of the early
signs of cellular degeneration in response to injury], of the
basal layer of epithelium.
mucous membrane pemphigoid intact basal layer
pemphigus vulgaris acantholysis
36. Single oral ulcer:
The most common cause of single ulcers on the oral mucosa
is trauma Traumatic ulcer
the penetrating nature of the inflammation results in myositis
that leads to chronicity called Traumatic Ulcerative
Granuloma punched out with surrounding tissue is
usually indurated, present for weeks or months.
Infections that may cause a single chronic oral ulcer;
- deep mycoses; histoplasmosis, blastomycosis and
mucormycosis.
- chronic herpes simplex infection.
- Syphilis cause a single oral ulcer in the primary and tertiary
stages.
37. Necrotizing sialometaplasia
benign, self-limiting, reactive inflammatory disorder of the
salivary tissue. Clinically, this lesion mimics a malignancy.
The etiology is unknown, although it likely represents a
local ischemic event, infectious process, or perhaps an
immune response to an unknown allergen
This is a self-limiting condition lasting approximately 6
weeks. No specific treatment is required, but débridement and
saline rinses may help the healing process.
Diagnosis requires an adequate biopsy specimen
