Recurrent ulceration

Recurrent aphthous ulceration of unknown aetiology is a common oral mucosa disorder affecting 20% of the population. It consists of recurrent bouts of one or more rounded, shallow, painful ulcers recurring at intervals of days to a few months.

Minor aphthous ulcers are the most common. They are less than 10 mm diameter, have a grey/white centre with a thin erythematous halo and heal within 14 days without scarring. Major aphthous ulcers are larger (more than 20 mm diameter), often persist for weeks or months and heal with scarring.

Most patients with recurrent ulcers are otherwise well. Various nutritional deficiencies of iron, folic acid or vitamin B12 (with or without gastrointestinal disorders) are occasionally found.

Box 6.2 Causes of halitosis

Poor oral hygiene Anxiety when halitosis is more imaginary than real Rare causes: oesophageal stricture pulmonary sepsis

There are no specific, effective therapies. Corticosteroids may lessen the duration and severity of the attacks. Chlorhexidine gluconate mouthwash, dapsone, colchicine, systemic steroids and azathioprine have all been used with variable effect.

Ulceration associated with systemic disorders

Oral ulceration is seen in gastrointestinal disorders, such as Crohn’s disease, ulcerative colitis and coeliac disease in approximately 10-20% of cases. Other diseases associated with oral ulceration include lupus erythematosus (systemic and discoid), Behçet’s disease, neutropenia and immunodeficiency disorders. In Reiter’s disease, ulceration occurs in approximately 25-30% of patients.

Ulceration associated with dermatological disorders

These include erythema multiforme major, toxic epidermal necrolysis, lichen planus, pemphigus vulgaris, bullous pemphigoid, ‘epidermolysis bullosa’ and dermatitis herpetiformis.

Ulceration associated with viral infection

Herpes simplex virus.

Primary herpes simplex (usually type I but rarely type II) presents with fever and widespread confluent painful ulcers. After resolution, the virus remains latent and recurs as herpes labialis.

Coxsackie.

Hand, foot and mouth disease and herpangina, due to a different Coxsackie A, or rarely B, infection are described on page 50.

Other viruses.

Herpes zoster and cytomegalovirus are among many viruses that can produce mouth ulceration, usually during the acute infective phase.

Ulceration associated with bacterial infection

Syphilis and tuberculosis can rarely cause oral ulcerations and are seen mainly in developing countries.

Ulceration associated with drugs

Certain drugs can cause oral lichenoid eruptions. They include antimalarials, methyldopa, tolbutamide, penicillamine and gold salts.

Trauma

Traumatic ulcers may be due to ill-fitting dentures, tooth brushing or lacerations by sharp teeth.
Neoplastic lesions (squamous cell carcinoma)

Malignant tumours of the mouth account for 1% of all malignant tumours in the UK. The majority develop on the floor of the mouth or lateral borders of the tongue. Early tumours may be painless, but advanced tumours are easily recognizable as indurated aphthous ulcers with raised and rolled edges. Aetiological agents include tobacco, heavy alcohol consumption and the areca nut. Intra-oral lesions which undergo malignant transformation include leucoplakia, lichen planus, submucous fibrosis and erythroplakia (a red patch). The previous male predominance has declined. Treatment is by surgical excision and/or radiotherapy.

In some infections such as chickenpox the clinical presentation is so distinctive that no investigations are normally necessary to confirm the diagnosis. Other cases require investigation.

Box 2.1 Infections commonly associated with a rash

Macular/maculopapular Measles Rubella Enteroviruses Human herpesvirus 6 Epstein-Barr virus Cytomegalovirus Parvovirus Human immunodeficiency virus (HIV) Dengue Typhoid Secondary syphilis Rickettsia – spotted fevers Vesicular Chickenpox (herpes zoster virus) Shingles (herpes zoster virus) Herpes simplex virus Hand, foot and mouth disease (Coxsackie virus) Herpangina (Coxsackie virus) Petechial/haemorrhagic Meningococcal septicaemia Any septicaemia with disseminated intravascular coagulation (DIC) Tick typhus Viruses (Table 2.23) Erythematous Scarlet fever Lyme disease (erythema chronicum migrans) Toxic shock syndrome Urticarial Toxocariasis Strongyloidiasis Schistosomiasis Cutaneous larva migrans Others Tick typhus (eschar) Primary syphilis (chancre) Anthrax (ulcerating papule)

General investigations (to assess health and identify organ(s) involved)

These will vary depending on circumstances:

• Blood tests. Routine blood count, ESR and C-reactive protein, biochemical profile, urea and electrolytes are performed in the majority of cases (Box 2.2).
• Imaging. X-ray, ultrasound, echocardiography, CT and MR scanning are used to identify and localize infections. Biopsy or aspiration of tissue for microbiological examination may also be facilitated by ultrasound or CT guidance.
• Radionuclide scanning after injection of indium- or technetium-labelled white cells (previously harvested from the patient) may occasionally help to localize infection. It is most effective when the peripheral white cell count is raised, and is of particular value in localizing occult abscesses.

This is a general term to describe corneal inflammation. Common causes include herpes simplex virus, contact lens-associated infection and blepharitis. Symptoms include the sensation of a foreign body or pain (depending on the size and depth of the ulcer), photophobia and lacrimation. Vision is reduced if the ulcer is in the visual axis.

Herpes simplex keratitis

Corneal epithelial cells infected with the virus eventually undergo lysis and form an ulcer which is typically dendritic in shape. The ulcer stains with fluorescein and can be observed easily with a blue light. Topical immunosuppression, e.g. steroid drops, or systemic immunosuppression, e.g. AIDS, can lead to the centrifugal spread of the virus such that the ulcer increases in area and is referred to as a geographic ulcer. Recurrent attacks of HSV keratitis can be triggered by ultraviolet light, stress and menstruation. All these factors are responsible for activating the virus, which normally lies dormant in the ganglion of the V nerve.

Treatment

Aciclovir ointment five times a day for 2 weeks is usually very effective.

Contact lens-related keratitis

A small number of contact lens wearers develop infective corneal ulcers which are potentially sight-threatening. The organisms usually responsible include Gram-positive and Gram-negative bacteria. Patients should be referred to an ophthalmologist for scraping of the ulcer and commencement of antibiotic treatment.

Blepharitis

This is an extremely common condition where the lid margins are inflamed. Common underlying causes of blepharitis include meibomian gland dysfunction, seborrhoea and Staphylococcus aureus. Patients can be asymptomatic or complain of itchy, burning eyes because of tear film instability resulting from meibomian gland dysfunction. Staphylococcus aureus is frequently responsible for chronic blepharo-conjunctivitis and some patients may develop keratitis.

Treatment

Lid hygiene is the mainstay of treatment as it helps to reduce the bacterial load and unblock meibomian glands. A short course of topical chloramphenicol is useful in chronic cases but in severe cases or cases where acne rosacea is suspected, oral doxycycline may be required. Patients with keratitis should be referred to the ophthalmologist as they will require topical steroids.

Herpes simplex virus (HSV) occurs as two genomic subtypes. HSV type 1 is spread by direct contact and droplet infection. Most people are affected in early childhood but the infection is usually subclinical. Occasionally it can cause a self-limiting pyrexial primary illness with either clusters of painful blisters on the face or a painful gingivostomatitis. Once infected, cell-mediated immunity develops. In some individuals this response is poor and they may get recurrent attacks of HSV, often manifest as cold sores. Immunosuppression can also cause a recrudescence of HSV. HSV can also autoinnoculate into sites of trauma and present as painful blisters/pustules. For example they may be seen on the fingers of healthcare workers (’herpetic whitlow’).
HSV type 2 infections occur mainly after puberty and usually affect the genital area. Infections are often symptomatic and transmitted sexually. However, HSV type 1 can also be found in the genital area due to orogenital contact.

Other rare complications of HSV infection include corneal ulceration, eczema herpeticum (p. 1327), chronic perianal ulceration in AIDS patients and erythema multiforme.

Treatment

Oral valaciclovir (500 mg twice daily for 5 days) is used for primary HSV and painful genital HSV. Recurrent cold sores are treated with aciclovir cream but this must be used early to be effective in shortening an attack. Attacks of genital herpes become less frequent with time. Intravenous aciclovir must be used in immunosuppressed patients.

Adenoviral conjunctivitis

This is highly contagious and can cause epidemics in communities. Transmission is through direct or indirect contact with infected individuals. The onset of symptoms may be preceded by a cold or flu-like symptoms. The eye becomes inflamed and this is commonly associated with chemosis, lid oedema and a palpable preauricular lymph node. Some patients may develop a membrane on the tarsal conjunctiva and haemorrhage on the bulbar conjunctiva. Viral conjunctivitis can cause deterioration in visual acuity owing to corneal involvement (focal areas of inflammation). In 50% of the patients the conjunctivitis is unilateral.

Treatment

The condition is largely self-limiting in the majority of cases. Lubricants together with a cold compress can be soothing for patients. Strict hygiene and keeping towels separate from the rest of the household goes a long way in reducing the spread of the infection. Clinicians also need to ensure good hygiene practice to reduce cross-infection and infecting themselves. In patients with corneal involvement or intense conjunctival inflammation, topical steroids are indicated.

Herpes simplex conjunctivitis

Primary ocular herpes simplex conjunctivitis is typically unilateral. It usually causes a palpable preauricular lymph node and cutaneous vesicles develop on the eyelids and the skin around the eyes in the majority of patients. Over 50% of these patients may develop a dendritic corneal ulcer. The organism responsible for this condition is the herpes simplex virus (HSV), which is usually HSV-1 but HSV-2 can give rise to ocular infection.

Treatment

Primary ocular HSV infection is a self-limiting condition but most clinicians choose to treat it with topical aciclovir in order to limit the risk of corneal epithelial involvement.

Molluscum contagiosum conjunctivitis

This is typically unilateral and produces a red eye that generally goes unrecognized and comes to the forefront because patients fail to improve and the cornea starts to become involved. A closer look at the eyelids and the margin will reveal pearly umbilicated nodules and these are filled with the DNA poxvirus. A high index of suspicion is needed to make an early diagnosis.

Treatment

This includes curetting the central portion of the lesion, freezing the centre or completely excising the lesion. If the corneal involvement is severe or the eye is very inflamed, a short course of topical steroids such as prednisolone 0.5% or dexamethasone 0.1% is helpful.