Australian Dental Journal

Australian Dental Journal The official journal of the Australian Dental Association Australian Dental Journal 2010; 55:(1 Suppl): 14 22 doi: 10.1111/j.1834-7819.2010.01195.x The patient with recurrent oral ulceration AA Talacko,* AK Gordon,* MJ Aldred* *Dorevitch Pathology, Heidelberg, Victoria. ABSTRACT This paper discusses the range of recurrent oral ulceration which affects the oral mucosa. Types of ulceration covered in this paper include traumatic, infective, aphthous, ulceration related to the oral dermatoses, drug-induced, ulceration as a manifestation of systemic disease and ulceration indicating malignancy. Aspects of the aetiology, diagnosis and management of common oral recurrent ulcerative conditions are reviewed from a clinical perspective as an aid to practising dentists. Keywords: Ulceration, aetiology, diagnosis, clinical features, histopathological features, treatment. Abbreviations and acronyms: ANUG = acute necrotizing ulcerative gingivitis; HHV-1 = human herpes virus-1; LE = lupus erythematous; MMP = mucous membrane pemphigoid; RAU = recurrent aphthous ulceration. INTRODUCTION The diagnosis and management of the patient with recurrent oral ulceration requires a systematic approach based on the principles of taking an adequate history, clinical examination, investigations as appropriate, institution of management and, finally, review to allow for any necessary modifications of that management. It is worthwhile to begin with a definition of an ulcer: an ulcer is a complete breach of the epithelium. This becomes covered with a fibrin slough and appears as a yellow white lesion surrounded by erythema. DISCUSSION History It is assumed that the patient will be complaining of ulcers. Patients (and sometimes referring practitioners) may use the term loosely to include red lesions, normal structures such as the lingual tonsil and foliate papillae or the circumvallate papillae of the tongue and a feeling of ulcers. It is important at this stage of the proceedings to establish the precise nature of the patient s complaint. Assuming that it can be established that the patient is describing ulcers, as opposed to other lesions, the history of the present complaint can be elicited. The age of the patient may be of relevance in relation to the age of onset of the ulceration. A child or adolescent presenting with recurrent oral ulceration may pose a different diagnostic and management dilemma compared to an older patient. Some types of recurrent oral ulceration have a typical onset in childhood or adolescence (such as recurrent aphthous ulceration stomatitis). This pattern of oral ulceration can sometimes present in later life but a middle-aged or elderly patient presenting with recurrent oral ulceration should also raise other diagnostic possibilities such as lichen planus and vesiculobullous disorders. The duration of the ulceration is partly related to the age of onset and age at presentation and will also depend upon whether the ulcers are persistent or intermittent. Persistent ulceration may include recurrent oral ulceration but patients may need assistance in clarifying whether their ulcers are persistent by virtue of successive ulcers appearing over a period of time or persistence of a single ulcer or multiple lesions. A more typical pattern of recurrent oral ulceration will be characterized by periods of ulceration with remissions between bouts of ulceration. The progression of the ulceration since onset can be helpful in establishing whether the ulceration is becoming more severe. Assuming that there are multiple ulcers, their number, size, shape and location are important factors in establishing a diagnosis. Some patients complain of an altered sensation prior to ulcer development which is known as a prodromal phase. The patient may have had previous opinions and details of previous investigations and diagnoses should 14 ª 2010 Australian Dental Association

Recurrent oral ulceration be sought. Similarly, any previous proprietary or prescribed treatments should be elicited. It is helpful to establish whether there has been any benefit from any of these treatments. Because some patients with recurrent oral ulceration may have extraoral manifestations, questions should be directed to any skin involvement or other systems being affected such as the eyes or genital regions, which would raise a clinical suspicion of Behçet s syndrome. Some patients with recurrent oral ulceration may have a vesiculobullous disorder and questioning regarding any awareness of blistering before the ulcers appear should be pursued. At this stage it is reasonable to ask the patient whether they have any ulcers present at the time of the consultation. If this is not the case then a presumptive diagnosis can be made at the end of the initial consultation and the patient reviewed when the ulcers next appear. Medical history Many patients with recurrent oral ulceration are in good health but some may have pre-existing medical problems which may be of relevance. These may include anaemia, blood dyscrasias, autoimmune disease and diabetes. The medical history will include ascertaining any medication taken by the patient. Some medications are associated with oral ulceration, e.g., methotrexate. 1 Dental history Oral ulceration which appears after dental treatment can be an indicator of minor recurrent aphthous ulceration. Minor trauma to the tissues can precipitate ulcers in susceptible patients. Some patients may report a crop of ulcers at the same site in the mouth occurring after dental treatment. This may occur in the palate or buccal sulcus and would raise a suspicion of recurrent intraoral herpes simplex virus infection effectively an oral cold sore. the buccal labial mucosa and lateral and ventral surfaces of the tongue. In a patient with herpetiform ulceration, multiple pinpoint ulcers would typically be seen on the non-keratinized mucosa with the possibility of more ragged ulcers by virtue of adjacent ulcers enlarging and fusing. Major aphthous ulcers tend to be larger (>10 mm diameter) and are more commonly seen in the oropharynx; they heal with scarring. Erythema of the buccal mucosa and or lateral ventral surfaces of the tongue with superimposed striae would be typical of lichen planus and this may become ulcerated by breakdown of the erythematous (eroded) epithelium into an irregular ulcer. A pattern of more ragged ulceration, perhaps with peeling of the adjacent epithelium, would raise the possibility of a vesiculobullous disorder, such as mucous membrane pemphigoid or pemphigus vulgaris. Clinical distinction between the two can be difficult but in pemphigus vulgaris the vesicles are short-lived and therefore infrequently seen, whereas in mucous membrane pemphigoid the blisters, by virtue of their full-thickness roof, can persist for longer. Bleeding, crusting and ulceration of the lips should raise a suspicion of erythema multiforme. Ulcers related to a denture margin may also come within the category of recurrent oral ulceration. In such a case it may simply be a recurrent traumatic ulcer related to the denture. Alternatively, the presence of the denture could localize recurrent minor aphthous ulceration, lichen planus or a vesiculobullous disorder. At this stage, it may be possible to establish a provisional diagnosis based on the history and examination. Specific investigations may be performed; these may comprise haematological investigations. If there are no ulcers at the time of the consultation, the provisional diagnosis will be based on the history alone and the patient should be asked to return when the ulcers next appear. This requires some flexibility in appointments so that the patient can be seen in the period when the ulcers are present. Examination Extraoral examination should focus on general appearance including a crude measure of nutritional status. Assessment of skin and conjunctival pallor may assist in identifying anaemic patients. The regional lymph nodes should be palpated as these may be enlarged in the case of persistent or large ulcers. Intraoral examination should assess the presence or absence of ulcers. The number, shape, size and location of the ulcers should be recorded. The presence or absence of scarring should be established. Minor recurrent aphthous ulceration will tend to present with several more or less circular ulcers on Causes of oral ulceration Trauma Traumatic ulceration may be recurrent if the offending irritant is not removed. The irritant may be mechanical, thermal or chemical in nature. Viral infection Recurrent intraoral viral infection is usually limited to secondary herpes simplex virus. The recurrences are most commonly due to human herpes virus-1 (HHV-1) (which usually causes orofacial infections). Recurrent ª 2010 Australian Dental Association 15

AA Talacko et al. oral HHV-2 lesions (which are usually associated with genital infections) are rare. Clinically, the initial presentation is of fluid-filled vesicles which rapidly break down to form a cluster of small ulcers with ragged margins. After primary infection, the virus is not eliminated from the body but migrates along nerve fibres to the trigeminal ganglion, where it lies dormant. In perhaps one-third of individuals the virus can be reactivated by non-specific stimuli, e.g., illnesses associated with fever, when it travels back to the periphery to cause secondary oral mucosal lesions. The lesions usually resolve in about 7 to 10 days in healthy individuals, but in immunocompromised patients secondary herpetic lesions can be widespread, very slow to heal and refractory to treatment. Other viral infections occurring in the mouth are due to varicella-zoster virus and coxsackie virus. These infections may become recurrent if the patient is immunocompromised. Ulceration due to bacterial infection, as in acute necrotizing ulcerative gingivitis (ANUG), may be recurrent. In this case, the successive bouts of ulceration along the gingival margins lead to blunting of the interdental papillae. ANUG tends to be more prevalent in winter months and there is an association with smoking. Recurrences may be more likely if the patient has compromised general health. (a) (b) Fig 1. Drug-induced ulceration of the tongue (a) and palate (b). Nutritional deficiency A nutritional deficiency such as a deficiency of iron, folate or vitamin B12 may predispose the patient to recurrent oral ulceration and it may aggravate RAU. Gastrointestinal disease Gastrointestinal disease such as coeliac disease, Crohn s disease, ulcerative colitis or a malabsorption syndrome can present with recurrent oral ulceration. Haematological disorders Haematological disease such as leukaemia, pancytopaenia, aplastic anaemia or agranulocytosis may present clinically with ulceration but this ulceration is unlikely to be recurrent. Medications A number of medications, e.g., methotrexate may have a side-effect of oral ulceration (Fig 1). This sideeffect may be dose-related. However, do not automatically assume that any medication being taken by a patient with oral ulceration is the cause of their ulcers. Xerostomia Xerostomia may predispose to recurrent oral ulceration, especially if dentures are worn. The xerostomia may be multifactorial in origin and may be due to autoimmune disease such as Sjögren s syndrome or the side effects of medications such as antidepressant medications. Neoplastic disease Although oral neoplastic disease may present with oral ulceration, the ulceration is persistent and progressive in nature. Specific conditions to consider Recurrent aphthous ulceration (RAU) is the most common form of recurrent oral ulceration, reportedly affecting up to 20% of the population. In most patients, the ulcers first appear in childhood or adolescence; there may be a slight female predisposition and in some patients there is a family history of similar ulceration which suggests a genetic factor. The aetiology of the condition is not completely understood but is thought to be immunologically-based. Factors that predispose to or precipitate the disease are more fully understood 16 ª 2010 Australian Dental Association

Recurrent oral ulceration and identification and elimination of these factors may be useful in management of the patient. Recurrent aphthous ulceration can occur in three forms: (1) Minor recurrent aphthous ulceration this is the most common form, accounting for approximately 80 90% of cases. The ulcers are usually round or oval and occur on the non-keratinized oral mucosa. Thus, they tend to occur on the lip and cheek mucosa and lateral margins of the tongue, sparing the dorsum of the tongue, palate and gingivae. In the buccal or labial sulcus the ulcers may be linear (Fig 2). One to five ulcers usually occur at a time and they are approximately 5 mm in diameter. The ulcers heal without scarring after 1 to 2 weeks and then recur, usually at intervals of a few weeks or months, although some patients are rarely without ulcers. (2) Major recurrent aphthous ulceration this form is much less common and accounts for about 5 10% of cases. The ulcers are similar to those of minor recurrent aphthous ulceration, but occur on any part of the oral mucosa including keratinized regions such as the hard palate and dorsum of the tongue as well as the oropharynx and can be larger than 10 mm in diameter (Fig 3). One or two ulcers generally occur at any one time. They tend to be persistent, lasting for at least one month, heal with scarring, and then recur. (3) Herpetiform ulceration this has a similar prevalence to major RAU. This form of ulceration begins as small round ulcers, approximately 1 mm in diameter (Fig 4), which are present in large numbers (up to 100). These coalesce to produce larger ulcers with irregular margins. They usually occur on the non-keratinized mucosa but any part of the oral mucosa may be affected. The ulcers can take up to two weeks to heal (without scarring) and later recur. Fig 3. A major aphthous ulcer on the soft palate. The ulcer is large and irregular in shape. Fig 4. Herpetiform ulceration on the lower lip mucosa. Some patients have ulceration which is intermediate between minor and major RAU, sometimes termed severe minor RAU. Although these ulcers commonly develop in childhood, some patients develop them later in life. All forms of aphthous ulceration produce significant discomfort and patients with severe minor aphthae, major aphthae or herpetiform ulceration may have difficulty eating and talking. Oral dermatoses These conditions largely comprise lichen planus, mucous membrane pemphigoid, pemphigus vulgaris and erythema multiforme, although less common conditions such as dermatitis herpetiformis also affect the mucosa and may present clinically as recurrent oral ulceration. Fig 2. Minor aphthous ulcers in the maxillary buccal sulcus. Note the erythematous margin. Lichen planus This condition has been estimated to affect 1% of the population, 2 being more prevalent with increasing age. It can occur as a skin or a mucosal disorder or may ª 2010 Australian Dental Association 17

AA Talacko et al. affect both skin and mucosa. The cause is unknown; the mechanism appears to be immunologically-mediated. Some drugs and other agents can cause lichenoid reactions, which are identical to lichen planus. Clinical features of lichen planus When lichen planus affects the oral mucosa, it may be asymptomatic or cause a range of symptoms from occasional minor discomfort to distressing pain some, all or most of the time. Asymptomatic lichen planus is often seen clinically as white lace-like patterns or plaques on uninflamed mucosa of the cheeks, tongue and sometimes the gingivae. Symptomatic lesions tend to have the typical striations or plaques on an erythematous mucosal base. The erythematous areas may merge into regions of ulceration which are invariably painful (Fig 5). Lichen planus may affect only the gingivae appearing as a desquamative gingivitis with erythema of the marginal and attached gingivae (Fig 6). This involvement of the gingivae is more extensive than the more common gingivitis due to poor oral hygiene and may be painful to varying degrees. There is a very small but recognized risk of malignant transformation in lichen planus, hence long-term review is recommended. Fig 6. Lichen planus presenting as a desquamative gingivitis. Diagnosis of lichen planus The clinical features of lichen planus often make it relatively simple to recognize, particularly if the lesions are bilateral and symmetrical, but it is advisable for the patient to have a biopsy for histopathological examination, including immunofluorescence. This will assist in the distinction between lichen planus and lupus erythematosus and white patches mimicking lichen planus, such as some dysplastic lesions. (a) Mucous membrane pemphigoid This autoimmune disease is uncommon and is often limited to the oral mucosa, but may also affect other mucosal surfaces including the conjunctiva to produce scarring (and sometimes blindness), hence the term cicatricial pemphigoid. (b) Clinical features of mucous membrane pemphigoid Mucous membrane pemphigoid (MMP) is a vesiculobullous disease which can cause lesions anywhere on the oral mucosa. It is more common in older patients, with some evidence of a female predilection. The vesicles may sometimes present as blood blisters. Although the vesicles are more robust than in pemphigus vulgaris, they tend to rupture within 24 hours to produce ulceration (Fig 7), which may heal with scarring. Occasionally only the gingivae are affected and appear red and inflamed in the absence of dental plaque (desquamative gingivitis). There may be little evidence of vesicle formation in these cases and the differential diagnosis will need to include lichen planus. Fig 5. Lichen planus presenting as ulceration surrounded by faint white striae on the ventral surface of the tongue (a) and erythema of the buccal mucosa (b). Diagnosis of mucous membrane pemphigoid The clinical features may be of assistance in establishing a diagnosis, but a definitive diagnosis can only be 18 ª 2010 Australian Dental Association

Recurrent oral ulceration Fig 7. A collapsed vesicle on the maxillary alveolar mucosa in a patient with mucous membrane pemphigoid. This has recently ruptured but will soon become an ulcer covered by a fibrin slough. reached by histopathological examination, including immunofluorescence. By this means, it will be seen that there is separation of the epithelium from the connective tissue at the level of the basement membrane zone and that the basement membrane zone in adjacent intact epithelium gives positive (usually IgG) immunofluorescence. Pemphigus vulgaris This is a relatively uncommon autoimmune disease, reported to have a greater prevalence in Ashkenazi Jews. In a significant number of cases, oral mucosal lesions are the first presentation of the disease. Clinical features of pemphigus vulgaris The disorder typically presents first in older patients. Patients develop thin-walled intraepithelial vesicles, which soon rupture. However, patients are often unaware of blistering because of the rapid breakdown to form ulcers (Fig 8). Diagnosis of pemphigus vulgaris Because of the often non-specific clinical appearance of the oral lesions, diagnosis is almost entirely dependent on histopathological examination including positive immunofluorescence findings. The characteristic histological finding is an intraepithelial split occurring close to the basal cells. Immunofluorescence is invariably positive for IgG around the prickle cells. Acantholytic cells (Tzanck cells) may be found in the vesicle fluid, either in sections or in smears from the lesions. Serological tests may demonstrate the presence of circulating autoantibodies. Erythema multiforme This is an acute onset disorder, which may be recurrent. The episode(s) may last for several weeks. It appears to be an immunological disorder of a hypersensitivity type in which immune complexes are formed and consequent tissue damage occurs. The condition is seen most commonly in adolescents and young adults and may be drug-induced or associated with an infection, commonly Herpes simplex or Mycoplasma pneumoniae. Clinical features of erythema multiforme When the skin is involved, typical target lesions may be produced, but when the mucosa of the mouth is the only site involved, the clinical appearance is often nonspecific. Widespread irregular shallow mucosal ulceration is usually present with sloughing and haemorrhage. The lips are often swollen, ulcerated and crusted with blood this is regarded as a sine qua non for diagnosis by some people (Fig 9). Stevens-Johnson syndrome is a more severe and generalized form of erythema multiforme, which involves the skin, oral mucosa, Fig 8. Ulceration of the tongue mucosa in a patient with pemphigus vulgaris. Fig 9. Erythema multiforme with extensive bleeding, ulceration and crusting of the lower lip. ª 2010 Australian Dental Association 19

AA Talacko et al. conjunctival and genital mucosa. The patient is febrile and unwell and requires hospital admission. Toxic epidermal necrolysis (Lyell syndrome) may represent the most severe end of the spectrum where epithelial necrosis is the predominant feature. Diagnosis of erythema multiforme Clinical features (particularly crusting and bleeding of the lips) and, in the case of recurrent episodes, associated events (such as recent medication or herpes labialis) will help establish a diagnosis. Histopathological examination with immunofluorescence will help to exclude other vesiculobullous disorders but is rarely diagnostic in itself. Discoid lupus erythematosus The first indication of this systemic disease can be the occurrence of oral mucosal lesions, but oral lesions in lupus are relatively uncommon. Lupus erythematosus (LE) is an autoimmune disease in which auto-antibodies are directed against nuclear components. Rare cases of drug-associated LE have been reported. Management of recurrent oral ulceration Diagnosis Ensure an accurate diagnosis has been made on the basis of a typical history and clinical appearance. Control trauma Eliminate or control possible sources of mucosal trauma, e.g., cheek or lip biting, overly vigorous brushing of teeth or using a hard toothbrush, sharp teeth dental prostheses or ingestion of sharp rough foods. Investigations Investigate for deficiency states, e.g., iron, folate or vitamin B12 deficiencies. A haematological screen should be carried out on all patients with RAU. If a deficiency is detected, the reason for the deficiency should be identified and corrected and supplement treatment instituted. If the deficiency is not corrected with supplements then referral to a gastroenterologist is recommended. Clinical oral features of lupus erythematosus LE is most commonly seen in older patients, with a female predilection. When it involves the oral mucosa it may have an appearance identical to that of oral lichen planus. It may appear as a relatively nondescript ulcer with an irregular outline, sometimes depressed below the level of the surrounding mucosa, and surrounded by erythematous mucosa, perhaps bordered by radiating white striae or white papules. Investigations of recurrent oral ulceration The investigations appropriate for a patient with recurrent oral ulceration will depend upon the provisional diagnosis. For patients with a provisional diagnosis of minor or major aphthous ulceration or herpetiform ulceration, haematological investigations should be instituted to exclude an anaemia or haematinic deficiency. A full blood count, iron studies, vitamin B12 and folic acid levels should be requested and any abnormalities investigated further and or corrected. Such haematological problems can precipitate oral ulceration and can aggravate ulceration in patients susceptible to aphthous ulceration. Should the provisional diagnosis include lichen planus and or a vesiculobullous disorder, a biopsy should be carried out, with tissue also removed for immunofluorescent investigations to assist in a firmer diagnosis. Biopsies are unproductive in minor and major aphthae and herpetiform ulceration. Diet Consider possible dietary factors and food sensitivities. 3 In occasional patients certain foods (e.g., oranges, eggs, wheat or dairy products) and other agents (e.g., cosmetics) can initiate or exacerbate RAU. A food diary may be helpful in identification of specific precipitating foods. Hormones In some female patients, RAU episodes appear to be related to their menstrual cycle. However, the evidence for a hormonal basis is inconsistent. Nevertheless, those patients who do report such an association may benefit from suitable hormone therapy. Psychological factors Psychological factors may be an important factor as some patients notice that their ulcers become worse in periods of illness, stress or extreme fatigue. Some form of stress management counselling may be considered in some of these cases. Medications If medication is a suspected cause of the recurrent oral ulceration, contact should be made with the patient s medical practitioner to discuss the possibility of prescribing an alternative medication. 20 ª 2010 Australian Dental Association

Recurrent oral ulceration Many treatments have been advocated for recurrent aphthous ulceration. These may be based upon antiseptics, antibiotics, corticosteroids, immunosuppressants, antirheumatics, anti-inflammatories, hormone therapy, antivirals, colchicine, thalidomide, pentoxifylline, sodium cromoglycate, interferon, hyaluronic acid, helicobacter eradication, zinc, various acids, gastric ulcer treatments, ultrasound, laser, cautery, cryotherapy, bioadhesives, herbal remedies, homeopathy, vitamins, lactobacillus as well as sundry other management strategies and combinations of various medications. 4 31 Systemic treatment may be appropriate for more severe and resistant cases. It should be made clear to the patient that the objective of treatment is symptomatic and that the ulcers cannot be cured. The plethora of treatments used for the treatment of oral ulceration is testament to the lack of any single effective treatment. There has not been a systemic (Cochrane) review of oral ulceration published. In their review, Porter and Scully 32 summarized the outcomes of a number of random clinical trials on oral ulceration. They reported that chlorhexidine could reduce ulcer severity and or duration but not incidence, steroids could reduce ulcer duration and may reduce pain. There is clearly a lack of robust data to allow a synthesis of published papers, hence the persistence of treatment based as much on empiricism as evidence. Despite the lack of clear evidence for any particular treatment for oral ulceration, some of the more widely accepted treatments used in oral medicine practice are outlined below: a 0.2% aqueous solution of chlorhexidine gluconate mouthwash used twice or three times daily while ulcers are present may provide relief in some mild cases. Alcohol-free mouthwashes will generally be more comfortable for the patient to use. Some clinicians believe that mouthwashes are more effective if used for 2 4 minutes at a time. Some patients find that topical local analgesics provide relief from symptoms and these may be offered if necessary. However, the use of such measures will affect the patient s sense of taste and the numbness may cause them to traumatize the oral mucosa, leading to further ulcers. Lignocaine 2% gel or mouthwash can be used for pain relief. This is especially helpful with extensive ulceration and major aphthous ulceration. Tetracycline mouthwashes were used for many years in recurrent oral ulceration, being particularly helpful when extensive ulceration is present. However, this preparation is no longer available in Australia. An alternative is to use minocycline, crushing a 50 mg tablet in 10 ml of warm water and using this as a mouthwash four times daily for five days. Concurrent antifungal treatment may be considered in patients with medical histories which might promote the development of an oral candidosis A number of corticosteroid preparations have been used in the treatment of recurrent oral ulceration. Ideally, these should be applied from the first indication of ulcer onset. Triamcinolone in Orabase 0.1% is often advocated for use on oral ulcers. It has the theoretical advantage of incorporating a corticosteroid in an adhesive base. However, some patients find this preparation difficult to apply and dislike the feel of the paste in the mouth. Betamethasone diproprionate OV 0.05% ointment or cream can be applied to the ulcers two or three times daily. Some patients do not like the sensation or taste of ointments and creams and some may have difficulty applying these oil-based preparations on a moist mucosal surface. The region(s) of ulceration should ideally be dried before application of the cream or ointment which can also be difficult and painful. A beclomethasone diproprionate 50 mcg dose or fluticasone proprionate 100 mcg dose asthma inhaler directed onto each ulcer (rather than inhaled) three or four times daily may be a convenient and effective means of medication application. A corticosteroid mouthwash may be helpful for widespread oral ulceration. This can be made from a 5 mg tablet of prednisolone crushed into 10 ml of warm water (or 1 ml of Redipred or Predmix in 10 ml water) or one dexamethasone 0.5 mg tablet in 10 ml water, the solution washed around the mouth and then expectorated. The immunosuppressant pimecrolimus 1% cream applied to lesions twice daily may be an effective alternative to other topical treatments. Intralesional injections of triamcinolone acetonide 10 mg ml are used by some clinicians for lesions of lichen planus. There is some discomfort in administering the medication and questions remain regarding the benefits after injections. A short course of systemic corticosteroids may occasionally be necessary in the management of major RAU and oral dermatoses. A logical treatment approach for patients with recurrent oral ulceration In patients in whom no predisposing factors are detected, chlorhexidine mouthwashes are an appropriate first line of treatment for recurrent oral ulceration. Topical corticosteroids used from the time of the earliest indication of prodromal symptoms provide symptomatic relief and reduce the duration of minor RAU and localized oral dermatoses. For more extensive ulceration, such as more severe minor RAU, herpetiform ulceration and oral dermatoses, topical minocycline or corticosteroid mouthwashes may be of assistance. Some patients with oral ulceration of various types may find benefit from using a chlorhexidine mouthwash followed by the use of an asthma inhaler. Occasionally systemic corticosteroids will be necessary, particularly in the management of major RAU, Behçet s syndrome and some patients with oral dermatoses. ª 2010 Australian Dental Association 21

AA Talacko et al. CONCLUSIONS It is essential to review the patient to assess their progress and response to any treatment instituted. It is important that patients are aware of the limitations of treatment. For example, patients with RAU need to be advised (and sometimes reminded) that a cure is not possible but that treatment is intended to reduce symptoms. This caution is also appropriate for lichen planus and the vesiculobullous disorders. Depending upon the response to treatment, alternatives could be trialled. REFERENCES 1. Kalantzis A, Marshman Z, Falconer DT, Morgan PR, Odell EW. Oral effects of low-dose methotrexate treatment. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2005;100:52 62. 2. McCartan BE, Healy CM. The reported prevalence of oral lichen planus: a review and critique. J Oral Pathol Med 2008;37:447 453. 3. Nolan A, Lamey PJ, Milligan KA, Forsyth A. Recurrent aphthous ulceration and food sensitivity. J Oral Pathol Med 1991;20:473 475. 4. 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Alidaee MR, Taheri A, Mansoori P, Ghodsi SZ. Silver nitrate cautery in aphthous stomatitis: a randomized controlled trial. Br J Dermatol 2005;153:521 525. 25. Arikan OK, Birol A, Tuncez F, Erkek E, Koc C. A prospective randomized controlled trial to determine if cryotherapy can reduce the pain of patient with minor form of recurrent aphthous stomatitis. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2006;101:e1 e5. 26. Kutcher MJ, Ludlow JB, Samuelson AD, Campbell T, Pusek SN. Evaluation of a bioadhesive device for the management of aphthous ulcers. J Am Dent Assoc 2001;132:368 376. 27. Babaee N, Mansourian A, Momen-Heravi F, Moghadamnia A, Momen-Beitollahi J. The efficacy of a paste containing Myrtus communis (Myrtle) in the management of recurrent aphthous stomatitis: a randomized controlled trial. Clin Oral Investig 2010;14:65 70. 28. Mousavi F, Mojaver YN, Asadzadeh M, Mirzazadeh M. Homeopathic treatment of minor aphthous ulcer: a randomized, placebo-controlled clinical trial. Homeopathy 2009;98:137 141. 29. Gulcan E, Toker S, Hatipoğlu H, Gulcan A, Toker A. Cyanocobalamin may be beneficial in the treatment of recurrent aphthous ulcers even when vitamin B12 levels are normal. Am J Med Sci 2008;336:379 382. 30. Gertenrich RL, Hart RW. Treatment of oral ulcerations with Bacid (Lactobacillus acidophilus). Oral Surg Oral Med Oral Pathol 1970;30:196 200. 31. Murphy GM, Griffiths WA. Aphthous ulcers responding to etretinate a case report. Clin Exp Dermatol 1989;14:330 331. 32. Porter S, Scully C. Aphthous ulcers (recurrent). Clin Evid 2005;13:1687 1694. Address for correspondence: Dr Anna Talacko and Dr Michael Aldred Dorevitch Pathology 18 Banksia Street, Heidelberg VIC 3084 Email: oralpathologists@dorevitch.com.au 22 ª 2010 Australian Dental Association