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CPD Article

Diagnosis and management of common non-viral oral ulcerations

Van Heerden WFP, BChD, MChD (Oral Path), FC Path(SA) Oral Path, PhD, DSc Department of Oral Pathology, University of Pretoria Boy SC, BChD, MChD (Oral Path) Department of Oral Pathology, University of Pretoria

Correspondence to: Prof Willie van Heerden, e-mail: [email protected]

Abstract

Oral ulcerations are common lesions encountered in private practice. Oral ulcers can have a localised aetiology or be a mani- festation of a variety of systemic conditions or disorders. Appropriate management depends on the correct diagnosis which can at times be difficult due to similar clinical features. The aetiology, diagnosis and management of the most common non-viral ul- cerative disorders of the are discussed. These include traumatic ulcers, recurrent aphthous , malignancy as well as oral ulceration associated with cutaneous pathology. SA Fam Pract 2007;49(8): 20-26

Introduction cally-associated ulcers is aspirin burns, 2. Persistent ulcers without vesicle Oral ulcerations are common lesions formation where acetylsalicylic acid-containing encountered in private practice. Oral • Gastrointestinal disease tablets or powders are placed directly ulcers can have a localised aetiology Crohn’s disease on the mucosa next to a carious tooth, or be a manifestation of a variety of sys- Ulcerative colitis resulting in various degrees of epithelial temic conditions or disorders (see Table • Haematological disorders necrosis. Thermal burns, as seen with I). Appropriate management depends Leukaemia Neutropaenia hot food, especially cheese (pizzas) and on the correct diagnosis, which at times • Rheumatoid Diseases tomatoes, are often seen on the can be difficult due to similar clinical DLE and tongue. Local radiotherapy and cer- features. Viral , many of which • Cutaneous disease tain chemotherapy regimens can cause present as ulcerative lesions, have been Ulcerative oral mucositis, which presents as multi- discussed in a previous edition.1 The • Drug reactions (may be preceded ple areas of painful , ulceration by vesicles) 2 aetiology, diagnosis and management 3. Ulcers with preceding vesicle and even epithelial sloughing. of the most common non-viral ulcerative formation disorders of the oral mucosa are dis- • Cutaneous disease Diagnosis cussed. These include traumatic ulcers, Traumatic ulcers, especially acute ul- recurrent , malignan- vulgaris cers, present with various degrees of cy, as well as oral ulceration associated • pain and other signs of acute inflamma- infections with cutaneous pathology. Varicella zoster infections tion. Chronic ulcers are usually painless. Patients are often aware of traumatic Table I: Classification of the more frequent Hand foot-and- disease ulcers and can reflect the episode of oral ulcers based on aetiology and trauma when questioned about it. These appearance ulcers are usually solitary in nature. Traumatic ulceration 1. Solitary ulcers Aetiology Management • Traumatic ulcerations Acute and chronic traumatic injury to the When the clinical suspicion of a trau- • Malignant neoplasms oral mucosa is common and frequently matic aetiology exists for an oral , Extranodal non-Hodgkins results in ulceration. Mechanical trauma the cause should be determined and, Metastatic tumours is the most common cause. These may if applicable, be removed. The patient • Infections be caused by dentures, accidental should be followed up for a maximum Tuberculosis trauma, when soft tissue gets trapped of two weeks and if no clinical sign of between the teeth, or physiological improvement is present, a to Deep fungal infections trauma, where the patient has a habit of exclude more serious possible aetiology 2. Recurrent ulcers that heal spontaneously cheek or biting (morsicatio buccalis is indicated. Sucking of ice at the time of Recurrent aphthous stomatitis or labialis). It may also be iatrogenically receiving chemotherapy is effective as a Beçhet’s syndrome induced by rotary instruments, removal prophylactic treatment, as it reduces the Reiter’s syndrome of dried cotton rolls from the mucosa or blood flow to the oral mucosa during the negative pressure from the saliva ejec- time of peak serum concentration. An- tor. The most common cause of chemi- tiseptic mouth washes (chlorhexidine)

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or anti-inflammatory washes (benzyda- Table II: Clinical features of RAS and comparison with herpes simplex ulceration mine) are often used as a treatment for 3 Primary her- Recurrent her- oral mucositis in patients. Minor Major Herpetiform pes simplex pes simplex aphthous aphthous aphthous ulceration ulceration Recurrent aphthous stomatitis (RAS) Age of <10 yrs, Aetiology 10–19 yrs 10–19 yrs 20–29 yrs adulthood Recurrent aphthous stomatitis is one of onset childhood the most common conditions leading to Non-kera- Keratinised Non-ke- Keratinised Keratinised recurrent oral ulceration. The aetiology tinised muco- plus non- ratinised non-movable mucosa, most for RAS is basically unknown. Several sa, especially keratinised mucosa, but bound mu- common on labial/buccal mucosa of particularly cosa, hard vermilion, occa- Site aetiological factors, including genetic mucosa, dor- particularly floor of mouth palate and sional gingiva predisposition, local trauma, hormonal sum and lat- and ventral gingiva and hard palate changes, infective agents, gastrointes- eral borders and lip surface of tinal disorders, stress, immunological of tongue tongue abnormalities and haematological de- 1–2 mm, 1–2 mm, Size 3–5 mm 5–15 mm 1–2 mm preceded by preceded by ficiencies (vitamin B12, red cell folate, iron), have been proposed.4 The ma- vesicles vesicles jority of patients, however, are healthy. >10, which >10, which Systemic conditions, including Beçhet’s Number 1–5 1–10 may co- may co- often only a few syndrome, and chronic malabsorption alesce alesce conditions, such as Crohn’s disease, ul- Duration 7–14 days >30 days 10–30 days 5–7 days 5–7 days cerative colitis and celiac disease, may be associated with RAS. Table III: Treatment options for RAS

Diagnosis Reassure the patient that: RAS affects between 15 to 25% of the • It’s a common condition, it’s not malignant, it has no healthy population. Males and females malignant potential and it’s not contagious or infec- are equally affected, with a peak in early tious No treatment Self-medication: adult life. It is more common in profes- • Covering agents like orabase sional and semi-professional people • Antiseptic mouthwashes (Corsodyl, Chlorhexidine) and is rarely seen in smokers. The ul- Avoid sharp and spicy foods and acidic or carbonated cers can arise every four to 12 weeks drinks and may be classified as minor, major Kenalog in orabase (triamcinolone) • Apply to dried ulcer with ear bud or moistened finger. and herpetiform, affecting approxi- Mild ulceration (ulcer-free • Allow to become wet before contact with uninvolved mately 80%, 10% and 5 to 10% of RAS period of one month or more) mucosa. Four times daily, one application before go- patients respectively. The diagnosis of ing to bed. For use where ulcers are accessible RAS is based on the history of recur- rences of painful, self-healing ulcers at Betamethasone mouthwash (Celestone 0.5 mg tab in 5–10 ml warmish water) regular intervals on non-keratinised mu- • Four times daily. Hold in mouth for 3 min and spit out cosa (labial, buccal, soft palate, ventral mouthwash (Meticorten 5 mg in 15 ml warm- surface of the tongue, floor of mouth and ish water) oro-) (see Figure 1). A biopsy is Moderately severe ulcer- • Four times daily. Hold in mouth for 3 min and spit out. ation (2–4 week ulcer-free It may also be applied to a small piece of cotton wool rarely indicated. The most important period) and this held over the lesion for longer differential diagnosis is with herpes 0.05% Fluocinonide in orabase (50/50) simplex -associated ulceration • Applied 6x pd to early ulcers (see Table II).5 Beclomethasone dipropionate aerosol (Beconase spray) 2 puffs (100 microgram) onto affected area. Maximum of 8 puffs/day Figure 1: Minor aphthous ulcer (arrow) on the ventral aspect of the tongue. Systemic corticosteroids • 30–60 mg daily for a week, followed by a one-week Severe ulceration (ulcer-free taper less than two weeks, all major (50–200 mg daily for four to eight weeks) RAS) has been used successfully in selected cases, but is rarely indicated due to severe side effects Referral is indicated Tetracycline 250 mg caps dissolved in 10 ml of warm- ish water as mouthwash Herpetiforme RAS • Hold in mouth for 3 min and then spit out. Three times daily. Not for children under 12. Evaluate patients for Candida overgrowth Management Reassure parents Ensure correct diagnosis About 20% of patients may have vitamin Children with RAS Ensure eating and hydration (parents) B12, red cell folate or iron deficiency, Local anaesthetic preparation on ulcer before eating and it is therefore best to exclude these More severe – Kenalog in orabase (children may need potential causes. These conditions are help with application)

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more likely to be present in older pa- has a characteristic appearance that and plaques.9 It is common for patients tients whose ulceration starts or worsens may serve as a diagnostic aid (see Fig- to have a mixture of these three pat- in middle age. Correcting the deficiency ure 2). It may be fixed to underlying soft terns. Reticular LP is the most common has been shown to bring rapid relief tissues and bone, and regional lymph- form and consists of bilateral, raised, for these patients. Treatment is mostly adenopathy may be present. Malignant delicate thin white lines that produce symptomatic, aimed mainly at pain re- ulcers are usually painless unless sec- a lace-like pattern set on an erythema- lief, reducing the frequency of ulceration ondarily infected. In advanced cases, tous background. These lesions are and preventing secondary infection. patients may present with or commonly seen on the buccal mucosa The choice of therapy depends on the impaired tongue movement. and are usually asymptomatic. Erosive severity and frequency of ulceration of the tongue may also present with ear LP presents with atrophic and erosive (see Table III). pain due to involvement of n. glossopha- areas on an erythematous background. ryngeus. Faint white striae can often be identified Malignant ulcers at the margin of the ulcers (see Figure Aetiology Figure 2: Squamous cell carcinoma present- 3). These lesions are painful and may A range of malignant neoplasms may ing as an indurated ulcer (arrow) be difficult to differentiate clinically from on the lateral border of the tongue. present as an ulcerative lesion, of which other erosive oral conditions, such as oral squamous cell carcinoma is by far mucous membrane pemphigoid and the most common. is a life- . Plaque LP pres- threatening disease in most countries, ents as white, flat to slightly raised ar- especially in developing countries. The eas, indistinguishable from . severity of oral cancer in South Africa is It is most commonly seen on the tongue. demonstrated by the fact that it is one of Patients may have other features of the most common malignancies in South lichen planus in the mouth that may help African males, a fact that is not often ap- to differentiate this lesion. It is usually preciated.6 One of the reasons may be asymptomatic. The clinical picture of LP that oral cancer is not registered as a is often characteristic, but the diagnosis single entity in the local cancer registry, should always be confirmed with an in- but separated into cancers originating cisional biopsy. from the mouth, tongue or . Oral Management cancer is largely a preventable disease, Any suspicious-looking oral mucosal Figure 3: Lichen planus presenting with as the primary aetiological agents are lesion, including any ulcer not healing white striae (arrow) on the buccal within two weeks after conservative mucosa that are combined with tobacco products, heavy use of alcohol, erosive red areas of ulceration and especially the combination of these treatment, must be biopsied to estab- (asterisk). two.7 More than 90% of oral cancer pa- lish the diagnosis. The biopsy should tients give a history of tobacco use. All be sufficiently large to include enough forms of tobacco use are implicated, abnormal and clinically normal tissue, including smokeless tobacco (chewing enabling the pathologist to make a diag- tobacco and snuff dipping).8 nosis without requesting additional ma- terial. After the diagnosis of oral cancer Diagnosis has been confirmed, the patient should Early detection of oral cancer allows be referred to a head and neck surgeon for a five-year survival rate of close to for further management and treatment, 90%. However, most oral cancers are which may vary from a localised exci- diagnosed at an advanced stage, with sion to extensive surgery with adjuvant a five-year survival rate of about 20%, chemo- and radiotherapy. which is one of the worst prognoses of Pemphigus vulgaris (PV) is an autoim- all major cancers. This is a tragic situa- Cutaneous disease mune disease characterised by an tion because no specialised techniques Aetiology antigenic attack and destruction of the are required to examine the oral cavity Ulcers may be a manifestation of several desmosomal attachment (intracellular for the presence of precursor lesions or diseases, the most common being cohesive system) of epithelial cells. This early oral cancers. Prevention and early lichen planus, pemphigus vulgaris results in epithelial separation above the diagnosis are therefore of the utmost erythema multiforme and mucous mem- basal cell layer, causing bullae on the importance. brane pemphigoid. skin and mucosae.10 The oral lesions Early cancerous lesions are usually precede cutaneous involvement in 75% painless and may appear as small, ap- Diagnosis of affected patients. Although lesions parently harmless areas of induration, Lichen planus (LP) is a chronic muco- may be confined to the oral cavity, the erosion or keratosis, often deceiving cutaneous disease in which skin and skin lesions usually develop in the sub- the unsuspecting clinician into a false oral lesions are seen simultaneously in sequent months. Failure to recognise sense of security. The advanced oral almost 40% of patients. Isolated skin the early oral lesion leads to a substan- cancerous lesion usually consists of a (35%) and mucosal (25%) lesions may tial delay in the diagnosis of this serious persistent painless ulcer with indurated, also be seen. LP presents with three dis- and life-threatening systemic disorder. rolled margins. In most cases the ulcer tinct clinical patterns: reticular, erosive Large and painful oral ulcerations are

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most commonly seen. Although these and may be confined to the oral cavity. tissue bands extending from the conjun- lesions start as bullae, they are soon lost The oral lesions are areas of painful ery- tiva of the eye to the sclera, and this can due to trauma during normal mastica- thema, bullae and ulcers, as well as ar- result in entropion and blindness. tion. All mucosal surfaces may be af- eas of bleeding and crusting (Figure 6). fected, but the soft palate is most com- The buccal mucosa, , soft palate and Figure 7: MMP presenting as desquama- monly involved, followed in order of fre- tongue are the most commonly involved tive of the gingival, with resulting ulceration (arrows). quency by the buccal mucosa, tongue sites. The clinical course of erythema and gingiva (see Figure 4). The use of a multiforme is usually over a period of blunt instrument will cause the epithelial three to four weeks. Recurrences are tissue to form a bulla and to separate, common, usually at intervals of several in both the skin and oral mucosa. This months over a period of years. Progres- is called the Nikolsky sign. Although this sion to more severe forms of EM (Steven sign is seen in other desquamative con- Johnson Syndrome and toxic epidermal ditions, it is more commonly seen in PV. necrolysis) sometimes occurs, with ex- The diagnosis should be confirmed with tensive systemic involvement. an incisional biopsy of an intact bulla, with inclusion of the adjacent normal Figure 5: Characteristic target lesions (ar- mucosa in order to evaluate the transi- rows) of erythema multiforme on the dorsum of the hand. tional zone. Management As LP is a chronic disease with no cure, Figure 4: Ulcerations with surrounding ery- treatment is aimed at symptomatic con- thema on the buccal mucosa (ar- rows) in a patient with pemphigus trol. If the patient is asymptomatic, no vulgaris. active treatment is required. For symp- tomatic atrophic or erosive lesions, treat- ment consists of topical steroids such as fluocinonide gel (0.05%) applied four to six times a day (mix with Orabase 1:1 to facilitate adhesion). Topical therapy affords only temporary control of the disease and patients should be advised Figure 6: Extensive ulceration and charac- that the lesions might recur. The devel- teristic crust formation (arrow) on opment of iatrogenic should the lips of the same patient with erythema multiforme be monitored and managed. Patients with PV should be referred for specialist treatment. Prolonged high dosages of systemic corticosteroids Erythema multiforme (EM) is an inflam- that are tapered as soon as control is matory disease of immune origin affect- obtained are still the mainstay of treat- ing the skin and mucosa. It arises due ment. Secondary infection of the ulcer- to immune complexes binding to vessel ated areas should be monitored and walls, with a subsequent inflammatory managed. process that leads to tissue loss. The The aetiological factor in EM should specific aetiology in a given patient is be eliminated if applicable. Mild cases often unknown, although herpes sim- of EM require only symptomatic treat- plex and certain drugs may be in- ment, which may include analgesics volved. EM is characterised by the rapid Mucous membrane pemphigoid (MMP) and anti-inflammatories such as aspi- onset of oral, cutaneous and ocular is an most com- rin or non-steroidal anti-inflammatory lesions. The skin lesions are discrete, a- monly seen in middle-aged to older drugs. However, care should be taken symptomatic, erythematous macules or females. It is characterised by bullous to check the history to ensure the EM sometimes vesicles that are distributed eruptions and ulceration, particularly was not precipitated by NSAIDs. Topi- in a symmetrical manner on the hands, of the oral mucosa and conjunctiva.11 cal steroids can also be prescribed. arms, legs, face and neck. These le- Eighty percent of the affected patients Minimising mucosal damage by means sions are known as bull’s-eye or target have oral lesions in the form of shallow of a bland liquid diet is essential. Main- lesions, appearing as a concentric ulcerations and a characteristic form of taining optimal oral hygiene to prevent erythematous patch with a peripheral gingivitis known as desquamative gin- secondary infections with agents such thin pale zone and a surrounding larger givitis (see Figure 7). Seventy percent as Candida is also important. erythematous zone (Figure 5). The cen- may have conjunctival lesions, 25% Treatment for MMP is similar to that tral small or bulla soon ruptures, have genital lesions, and 20% have skin of pemphigus vulgaris. Topical cortico- but heals rapidly, often leaving the red lesions. Involvement of the eye conjunc- steroids (fluocinonide gel 0.05%, mixed zone behind for a longer period. Skin tiva is a major concern. Bullae, erosions with Orabase) are indicated, especially lesions are pathognomic for EM. Oral and generalised swelling and erythema for gingival lesions. Systemic cortico- lesions are seen in 30 to 60% of cases, can lead to the formation of adhesive steroids are indicated in severe cases.

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Oral hygiene may be difficult for the pa- toto optimaloptimal managementmanagement andand treatmenttreatment tobacco. Adv Dent Res 1997;11:322–9. tient, given the . of such a patient. 9. Sugerman PB, Savage NW, Walsh LJ, et al. The pathogenesis of oral lichen planus. Crit Mouth washes containing agents such Rev Oral Biol Med 2002; 13: 350–365. as chlorhexidine are beneficial. Oph- See CPD Questionnaire, page 42 10. Black M, Mignogna MD, Scully C. Pem- thalmologic examination is important to phigus vulgaris. Oral Diseases 2005;11: evaluate and exclude the possibility of 119–30. P This article has been peer reviewed 11. Chan LS, Ahmed AR, Anhalt GJ, et al. The early ocular disease. Patients should first international consensus on mucous also be made aware of this in order to membrane pemphigoid. Arch Dermatol facilitate long-term management. References 2002;138:370–9. 1. Van Heerden WFP. Oral manifestations of Conclusion viral infections. SA Fam Prac 2006;48:20–4. 2. Porter SR, Leao JC. Review article: oral All patients with recurrent or persistent ulcers and its relevance to systemic dis- oral ulceration should be fully inves- orders. Aliment Pharmacol Ther 2005;21: tigated to establish a definitive diag- 295–306. nosis and to eliminate the possibility 3. Meade GM. Management of oral mucositis associated with cancer chemotherapy. of an underlying systemic disorder or Lancet 2002;359:815–6. oral malignancy. Ulcers should always 4. Scully C. Aphthous ulceration. N Engl J be examined for induration or fixation, Med 2006;355:165–72. which may be indicative of malignancy. 5. Field EA, Allan RB. Review article: oral ulceration – aetiopathogenesis, clinical Unless the cause is undoubtedly local, diagnosis and management in the gastro- general physical examination is always intestinal clinic. Aliment Pharmacol Ther indicated, looking especially for mu- 2003;18:949–62. cocutaneous lesions or other systemic 6. Van Heerden WFP, Butow K-W. The role of the dentist in the prevention and early diag- conditions. All undiagnosed ulcers, as nosis of oral cancer. S Afr Dent J 2002;57: well as ulcers that are suspected as 22–4. being malignant, should be biopsied. 7. Blot WJ, McLaughlin JK, Winn DM, et al. Although oral ulceration therefore may Smoking and drinking in relation to oral and pharyngeal cancer. Cancer Res 1988;48: pose a clinical dilemma, thorough clini- 3282–7. copathological examination will usually 8. Hoffmann D, Djordjevic MV. Chemical com- result in a final diagnosis that can lead position and carcinogenicity of smokeless

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