Ulcerative, vesicular and bullous lesions

Acute multiple oral lesions

Viral Infections Primary Herpes Simplex Virus, Coxsackievirus, Varicella-Zoster Virus infections

Incubation period

Generalized prodromal symptoms; fever, headache, malaise, nausea, vomiting, chills, anorexia

Vesicles

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

Primary HSV Infections

Primary HSV Infections (generalized acute marginal gingivitis)

Coxsackievirus Infections (Herpangina)

chickenpox, varicella

shingles, herpes zoster

Erythema Multiforme

Immune-mediated disease

Cell-mediated immunity

Deposition of immune complexes

The most common triggers for episodes of EM are; 1- herpes simplex virus2- 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

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.

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.

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.

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

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.

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.

Classic ANUG in patients without an underlying medical disorder is associated with three major factors:1. Poor oral hygiene.2. Smoking3. 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 .

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.

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

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.

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.

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

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.

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)

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.

Chronic multiple oral lesionsPemphigus vulgaris

binding of IgG autoantibodies to desmosomes

separation of cells [acantholysis]

destruction of desmosomescellular degeneration and suprabasilar bulla

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].

Patients with PV included in the differential diagnosis must have a biopsy done for;

routine histology direct immunofluorescence

indirect immunofluorescence

Mucous membrane pemphigoid:

autoantibodies basement membrane subepithelial split

vesicle

• Erosions typically spread more slowly than pemphigus lesions, more self-limiting, desquamative gingivitis

Patients with MMP included in the differential diagnosis must have a biopsy done for

routine histology direct immunofluorescence

indirect immunofluorescence

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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.

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

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.

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

Squamous cell carcinoma

Squamous cell carcinoma of the lateral border of the tongue

Necrotizing sialadenometaplasia on the palate

Two chancres on the tongue

Traumatic ulcer of the tongue

Major aphthous ulcer on the lower lip.

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