Phòng khám chuyên khoa da li�u - Thạc s� bác s� Hu�nh Văn Quang

Oral lesion

Introduction

Oral lesions can be the result of local disease, a manifestation of cutaneous disease or even a sign of systemic disease. Of the cutaneous diseases that affect the oral mucosa, some affect it as the presenting complaint (such as pemphigus vulgaris) and others affect it as the most persistent complaint (lichen planus). For a full skin examination to be complete it must include the oral cavity, an easily accessible and examinable mucosal surface. A wide variety of infections, developmental lesions, benign and malignant tumours can occur in the oral cavity, but the following discussion is limited to common presentations of oral disease.

Oral white patches

Introduction

White patches of the oral mucosa can be manifestations of physiological states, eg Fordyce’s spots, or pathological states, including: keratoses, eg idiopathic or frictional (at sites of occlusion), or associated with smoking; epithelial dysplasia; carcinoma; infections, eg candidiasis, syphilis or Epstein-Barr virus (EBV) infection in patients with the acquired immunodeficiency syndrome (AIDS); dermatoses, eg lichen planus, lupus erythematosus. The term leukoplakia is very nonspecific and implies the absence of a more specific diagnosis. It is defined as a persistent white patch or plaque, and is used irrespective of the presence or absence of epithelial dysplasia. Benign keratoses tend to be smooth plaques that have a low cancerous potential. Verrucous or speckled leukoplakia present as white patches on a red background and have a high risk of malignant change. Biopsy of any persistent, undiagnosed white oral patch is mandatory to exclude dysplasia, and in situ or invasive carcinoma.

Oral candidiasis

Oral candidiasis has many clinical presentations. Predisposing factors include immune suppression, corticosteroids, oral antibiotics, xerostomia and dentures. The creamy white patches of thrush are easily recognisable, but acute atrophic candidiasis (tender red mucosa after antibiotics) and chronic atrophic candidiasis (red gingiva due to dentures) are often misdiagnosed. Oral candidiasis can be diagnosed by microscopy of a swab specimen. See Oral and dental infections: fungal for treatment.It is essential that underlying predisposing factors are excluded, especially in recurrent cases. Local precipitants need to be corrected and oral hygiene should be addressed. For denture wearers with oral candidiasis, the antifungal agent should be applied to the fitting surface of the upper dentures. Dentures should be removed at night and soaked in a solution of sodium hypochlorite 1:100.

Oral hairy leukoplakia

Oral hairy leukoplakia presents with the lateral borders of the tongue matted by a ‘hairy’ white corrugation. The condition appears to be associated with EBV infection. This develops in patients who are immunosuppressed, and is most commonly seen in AIDS patients. Treatment of the oral lesion per se is not useful and management must address the underlying immunosuppression.

Oral lichen planus

Lichen planus is an immunologically mediated disease in which T-cells are directed against basal keratinocytes, causing an inflammatory rash with characteristic features. This inflammatory cutaneous disease frequently affects the mouth, with lesions typically on the buccal mucosa and tongue. White streaks forming a reticulated lacework is very characteristic. The lesions are often painful and sensitive to hot or cold food or drinks. Less commonly, ulcers and rarely bullae can occur. Oral lesions in lichen planus are associated with a persistent and protracted disease course, and are often difficult to treat. These persistent oral lesions can occur in the absence of any cutaneous lesions. Squamous cell carcinoma has been reported in areas of chronic erosive lichen planus, but the risk of this is very small. Nonetheless, regular review is important. While most oral lichen planus is idiopathic, some cases of oral lichenoid eruptions can be drug-induced, and rarely they may be associated with dental mercurial amalgams. In resistant cases, prior to considering any amalgam removal, it is essential that the patient is appropriately patch-tested to confirm any mercury hypersensitivity. Oral lichen planus can be treated with triamcinolone acetonide 0.1% paste OR other potent topical corticosteroids applied to the lesions OR stronger corticosteroid aerosols applied orally but not inhaled, 3 times daily after meals. In more persistent cases, use triamcinolone acetonide 10mg/mL OR betamethasone acetate/sodium phosphate 5.7mg/mL, 0.1 to 1mL intralesionally. If the oral disease is widespread or severe, or if associated with severe cutaneous lichen planus, useprednisolone 0.5 to 1mg/kg orally, daily for 4 to 6 weeks. Second-line therapies for severe lichen planus include oral acitretin,[Note] oral dapsone and topical or oral cyclosporin.

Geographic tongue This is a benign condition manifested by migratory areas of erythema, which can be quite sensitive. Histologically, there is epithelial thinning with an inflammatory infiltrate in the centre of the lesion. While the aetiology is unknown, there may be a family history of the condition and some patients have atopic allergies or can relate the lesions to particular foods or stress. It is occasionally seen in patients with psoriasis but is usually not associated with any other condition. Symptomatic relief can be obtained with topical analgesic oral preparations, eg choline salicylate, benzydamine, benzocaine or lignocaine.

Black hairy tongue Black hairy tongue is due to excessively long filiform papillae of the tongue being stained by an accumulation of epithelial cells, exogenous material and perhaps microorganisms. It can occur after courses of antibiotics. Suggested treatments include improved oral hygiene, brushing the tongue with a toothbrush, sodium bicarbonate mouthwashes and sucking a peach stone, pineapple or pawpaw.

Oral ulceration

Introduction

Mouth ulcers can be classified into 4 principal groups: infective (usually viral, occasionally bacterial or fungal), dermatological, neoplastic and other (including traumatic and aphthous).Ulcers persisting for more than 3 weeks without a known cause should be biopsied. See Table 1below for some common causes of oral ulceration.

Causes of oral mucosal ulceration (Table 1)

Oral ulceration: viral ulcers (including gingivostomatitis) Viral causes of oral ulceration include herpes simplex virus (primary herpetic gingivostomatitis) and coxsackie viruses (herpangina and hand, foot and mouth disease). Diagnosis of herpes simplex virus infection can be made on the basis of direct immunofluorescence or viral culture.Mild cases can be treated symptomatically with systemic analgesic and topical anaesthetic drugs, eg lignocaine gel. Chlorhexidine mouthwash may prevent secondary infection and act as an adjunct to oral hygiene. It is also available in combination with benzydyamine, a topical analgesic. Topical corticosteroids are contraindicated.In severe herpes simplex virus infections, particularly in primary and progressive infection and if the patient has difficulty eating or swallowing, antiviral therapy is recommended. Use

If unable to swallow, use

Aphthous ulcers Aphthae are common. In the simple form of the disease, ulcers are 2 to 4mm in diameter, they occur a few at a time and they heal in 1 week. A less common form produces larger lesions of 10mm that persist for 1 month and heal with scarring. Aphthae can be associated with deficiencies and 10% have low iron, folate or vitamin B₁₂. Three per cent of patients have coeliac disease. Aphthae can occur acutely with the cessation of smoking, but in this situation the condition tends to resolve spontaneously in time. Behçets syndrome is a rare condition featuring the association of aphthae with genital ulceration, eye disease and other systemic and cutaneous features. Assessment of aphthae involves the exclusion of underlying causes by history, examination and relevant blood tests. Recurrent oral ulceration is frequently due to aphthous ulcers after excluding underlying disease. Therapy is predominantly symptomatic. For mild disease topical anaesthetic agents, eg lignocaine gel every 3 hours, may be effective for symptomatic relief.Elimination of minor trauma, eg from tooth brushing or orthodontic appliances, should be emphasised. To reduce secondary infection and control plaque while the mouth is uncomfortable, use

Active treatment of lesions by the application of topical corticosteroid cream or ointment can produce rapid healing, particularly if applied in the prodromal phase.

For more severe ulcers betamethasone dipropionate 0.5 mg/g (0.05%) ointment or cream may be helpful.In major aphthous ulceration (only), a 5 day course of systemic oral steroids may be effective.

For severe ulceration in the immunocompromised patient specialist advice should be sought.

Pemphigus vulgaris Pemphigus vulgaris is an uncommon autoimmune bullous disorder that characteristically presents as large painful and persistent erosions in the mouth. This oral ulceration typically precedes the development of cutaneous lesions by 6 or more months. Almost all of the other autoimmune bullous diseases can cause oral bullae, which are usually seen as ulcers, but as a rule this is less frequent than with pemphigus vulgaris. Diagnosis is by histology and immunofluorescence of a biopsy. Treatment is often very protracted and usually requires oral immunosuppressive therapy with oral corticosteroids, azathioprine and cyclosporin, alone or in combination.

Erythema multiforme In erythema multiforme, the oral mucosa can be involved alone or in association with generalised skin lesions. Oral lesions begin as blisters, but are often seen only as large ulcerations on the mucosa or crusted erosions of the lips. Herpes simplex virus (HSV) is a common cause of erythema multiforme, so a history of HSV infection should be sought. Sometimes, even when HSV is shown to be the cause, the history of the infection may be forgotten or deemed unimportant because the lesions were trivial or minimal. Recurrent and severe erythema multiforme due to HSV may be controlled by the use of aciclovir, famciclovir or valaciclovir orally as prophylaxis, see Viral infections. Severe erythema multiforme and Stevens-Johnson syndrome are very likely to be due to a drug reaction and, consequently, a careful drug history must be obtained, see Drug eruptions. Maintaining oral hygiene is paramount. Oral toilets in the early phases can be replaced by gentle warm saline mouthwashes in the later phases. In severe cases, particularly in drug-associated erythema multiforme/ Stevens-Johnson syndrome, early intervention is required, with cessation of the causative drug and institution ofprednisolone 0.5 to 1.0mg/kg orally, daily for 1 to 2 weeks then reduced and ceased over 1 to 2 weeks.

Angular cheilitis This is an inflammation of the skin and labial mucous membrane at the angles of the mouth. Important factors in the aetiology of this condition are: infection, mechanical factors, dermatoses, nutritional deficiencies. Candida and staphylococci are the most common causes, with Candida being the single most likely infective agent. Candidal angular cheilitis is particularly associated with denture wearing. There may be symptomatic chronic atrophic candidal gingivitis beneath the denture. If oral Candida is present, it is essential that this be treated.

However, recurrence is common. The patient should be advised against perpetuating the lesions by licking the corners of the mouth and appropriate alterations to denture hygiene are essential. For unilateral angular cheilitis in the absence of oral candidiasis, staphylococcal infection should be suspected, see Impetigo.The angular fold becomes deeper as a consequence of ageing and in edentulous patients if dentures are not used. Saliva can accumulate in this fold, producing maceration and eventually cheilitis. New dentures may help correct this excessive folding, and dental review is helpful. If frequent wearing of dentures does not correct the lateral commissure overhang, surgery to reduce the angular fold may be worthwhile. Atopic and seborrhoeic dermatitis can produce an angular cheilitis. A variety of nutritional deficiencies, including riboflavin, iron and folate, can produce this cutaneous sign. Riboflavin deficiency can also produce shiny red lips, and iron, folate and vitamin B₁₂ deficiencies will cause an angular cheilitis associated with atrophic glossitis. Salivary dermatitis Prolonged or intermittent and repetitive exposure of a nonmucosal cutaneous surface to saliva will cause irritation and ultimately an irritant contact dermatitis. This is observed in patients in vegetative states, particularly where saliva accumulates in deep angular folds. It also occurs in ‘lip-licking dermatitis’ seen most commonly in young children and teenagers. Dry and chapped lips are moistened by the licking of the lips. This, however, produces more irritation, and a well-defined erythematous and slightly scaly area of dermatitis develops on the perivermilion area of the upper and/or lower lip. Education of the patient/carer regarding the cause of the rash is useful, so that steps can be taken to limit the lip-licking habit. The skin must be protected from saliva and any chapping treated with white soft paraffin applied frequently to lips and corners of mouth. The erythema and irritation can be treated with hydrocortisone 1% ointment applied 2 to 3 times daily.

• < Trước
• Tiếp tục >