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.

adolescent presenting with recurrent oral 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
14
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 dura-
tion 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 ulcer-
ation but patients may need assistance in clarifying
whether their ulcers are persistent by virtue of succes-
sive ulcers appearing over a period of time or persis-
tence 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
ª 2010 Australian Dental Association

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 manifes-
tations, 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 ascer-
taining 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’’.
Examination
Extraoral examination should focus on general appear-
ance 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
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Recurrent oral ulceration
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 possibil-
ity 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 vesiculo-
bullous disorder, such as mucous membrane pem-
phigoid 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-thick-
ness 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 recur-
rent 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 per-
formed; these may comprise haematological inves-
tigations. 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.
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
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AA Talacko et al.

oral HHV-2 lesions (which are usually associated with (a)

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 le-
(b)
sions 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 recur-
rent. 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 Fig 1. Drug-induced ulceration of the tongue (a) and palate (b).
has compromised general health.

Nutritional deficiency Xerostomia

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, pancyto-
paenia, aplastic anaemia or agranulocytosis may pres-
ent 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 side-
effect may be dose-related. However, do not auto-
matically assume that any medication being taken by
a patient with oral ulceration is the cause of their
ulcers.
16
Xerostomia may predispose to recurrent oral ulcera-
tion, 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
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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 Fig 3. A major aphthous ulcer on the soft palate. The ulcer is large
ulcers heal without scarring after 1 to 2 weeks and and irregular in shape.
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 preva- Fig 4. Herpetiform ulceration on the lower lip mucosa.
lence to major RAU. This form of ulceration begins
as small round ulcers, approximately 1 mm in
diameter (Fig 4), which are present in large num- Some patients have ulceration which is intermediate
bers (up to 100). These coalesce to produce larger between minor and major RAU, sometimes termed
ulcers with irregular margins. They usually occur severe minor RAU. Although these ulcers commonly
on the non-keratinized mucosa but any part of the develop in childhood, some patients develop them later
oral mucosa may be affected. The ulcers can take in life.
up to two weeks to heal (without scarring) and later All forms of aphthous ulceration produce significant
recur. 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.
ª 2010 Australian Dental Association
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
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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.
Fig 6. Lichen planus presenting as a desquamative gingivitis.
Symptomatic lesions tend to have the typical stria-
tions or plaques on an erythematous mucosal base. The
erythematous areas may merge into regions of ulcera-
Diagnosis of lichen planus
tion which are invariably painful (Fig 5). Lichen planus
may affect only the gingivae – appearing as a ‘‘desqua- The clinical features of lichen planus often make it
mative gingivitis’’ with erythema of the marginal and relatively simple to recognize, particularly if the lesions
attached gingivae (Fig 6). This involvement of the are bilateral and symmetrical, but it is advisable for the
gingivae is more extensive than the more common patient to have a biopsy for histopathological exami-
gingivitis due to poor oral hygiene and may be painful nation, including immunofluorescence. This will assist
to varying degrees. There is a very small but recognized in the distinction between lichen planus and lupus
risk of malignant transformation in lichen planus, erythematosus and white patches mimicking lichen
hence long-term review is recommended. planus, such as some dysplastic lesions.

Mucous membrane pemphigoid

(a) 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.

Clinical features of mucous membrane pemphigoid

Mucous membrane pemphigoid (MMP) is a vesiculo-
bullous 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
(b) vesicles may sometimes present as blood blisters.
Although the vesicles are more robust than in pemphi-
gus 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.

Diagnosis of mucous membrane pemphigoid

Fig 5. Lichen planus presenting as ulceration surrounded by faint
white striae on the ventral surface of the tongue (a) and erythema of The clinical features may be of assistance in establishing
the buccal mucosa (b). a diagnosis, but a definitive diagnosis can only be
18 ª 2010 Australian Dental Association

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 connec-
tive tissue at the level of the basement membrane zone
and that the basement membrane zone in adjacent
intact epithelium gives positive (usually IgG) immuno-
fluorescence.
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).
Fig 8. Ulceration of the tongue mucosa in a patient with pemphigus
vulgaris.
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Recurrent oral ulceration
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 histo-
logical 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 non-
specific. Widespread irregular shallow mucosal ulcera-
tion 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 9. Erythema multiforme with extensive bleeding, ulceration and
crusting of the lower lip.
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. Histopatholog-
ical 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.
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 provi-
sional 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 haemat-
inic 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 provi-
sional diagnosis include lichen planus and ⁄ or a vesicu-
lobullous disorder, a biopsy should be carried out, with
tissue also removed for immunofluorescent investiga-
tions to assist in a firmer diagnosis. Biopsies are
unproductive in minor and major aphthae and herpe-
tiform ulceration.
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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 prosthe-
ses 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.
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 pre-
scribing an alternative medication.
ª 2010 Australian Dental Association

Many treatments have been advocated for recurrent
aphthous ulceration. These may be based upon anti-
septics, antibiotics, corticosteroids, immunosuppres-
sants, antirheumatics, anti-inflammatories, hormone
therapy, antivirals, colchicine, thalidomide, pentoxifyl-
line, sodium cromoglycate, interferon, hyaluronic acid,
helicobacter eradication, zinc, various acids, gastric
ulcer treatments, ultrasound, laser, cautery, cryo-
therapy, bioadhesives, herbal remedies, homeopathy,
vitamins, lactobacillus as well as sundry other
management strategies and combinations of various
medications.4–31 Systemic treatment may be appro-
priate 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 Scully32 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 chlorhex-
idine 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 develop-
ment of an oral candidosis
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Recurrent oral ulceration
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 prep-
aration 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 pime-
crolimus 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 appropri-
ate 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.
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.
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Address for correspondence:
Dr Anna Talacko and Dr Michael Aldred
Dorevitch Pathology
18 Banksia Street,
Heidelberg VIC 3084
Email: oralpathologists@dorevitch.com.au
ª 2010 Australian Dental Association