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Demystifying Recurrent
Oral Ulcerations
A Peer-Reviewed Publication
Written by Michelle Hurlbutt, RDH, BS and Lane Thomsen, DDS, MS
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Educational Objectives
Upon completion of this course, the clinician will be able to
do the following:
1. Explain the etiology of oral ulcerations.
2. Describe the clinical features and symptoms of
aphthous ulcers.
3. Conduct a differential diagnosis for recurrent
oral ulcerations.
4. Outline the topical and systemic medications used in
the treatment of recurrent aphthous ulcerations and
other palliative care and recommendations for patients.
Abstract
Oral irritations and ulcerations occur frequently in the general
population. Recurrent aphthous ulcers (RAU) are the most
common. There are three types of RAU — minor, major and
herpetiform, the most common being minor aphthae. The
exact etiology of RAU is not known. Systemic and local factors, as well as infectious agents, have been proposed. Certain
medications and foods are associated with oral ulcerations,
and chemicals such as sodium lauryl sulfate (SLS) contained
in dentifrices have also been implicated. RAU also occur in
more serious systemic diseases and where appropriate patients
should be referred for screening and medical care. Treatment
of recurrent aphthous ulcers is palliative, based on the severity of the lesions. Both topical and systemic medications are
available. Nutritional and oral hygiene advice should also be
given, and if patients are sensitive to SLS, a low-dose SLS or
SLS-free dentifrice should be recommended.
include Behçet’s disease, inflammatory bowel disease, Sweet’s
syndrome, HIV infection, lupus, neutropenia, Mouth and
Genital Ulcers with Inflamed Cartilage Syndrome (MAGIC)
syndrome, mucous membrane pemphigoid, pemphigus vulgaris and erythema multiforme. It is essential that the clinician
understands the etiological factors and can perform a differential diagnosis for RAU to treat the patient appropriately.
Signs and Symptoms of
Recurring Aphthous Ulcers
Minor aphthous ulcers
Minor aphthous ulcers are small and cause the least discomfort. They are most prevalent in people 10–40 years of
age. Usual locations include the floor of the mouth, buccal
and labial mucosa, tip of the tongue, and ventral surface of
the tongue. They are rare on the dorsum of the tongue and
on keratinized mucosa. Patients may become aware of them
when a tingling or burning sensation occurs. Within two days,
a raised erythematous (red) papule or white spot appears.
This ulcerates, resulting in a pseudomembranous grayish or
yellowish center within the lesion. Minor aphthae are round
or oval and measure up to 4 mm in diameter. They usually
heal uneventfully seven to ten days after the first signs appear.
Recurrence may take weeks or years.9,10
Figure 1. Minor aphthous ulcer
Introduction/Overview
Oral irritations and ulcerations occur frequently in the general population and result in varying degrees of pain and
debilitation for patients. Recurrent aphthous ulcers (RAU),
also known as “canker sores,” are the most common.1 RAU
occur in approximately 20% of the population, with greater
prevalence in upper socioeconomic groups and nonsmokers.2
There are three types of RAU: minor, major and herpetiform.
The most common are minor aphthae, accounting for at least
80% of all cases.3,4 Major aphthae account for approximately
10% of cases, and herpetiform less than 10%.5,6 Usually patients only have one type.7
The second most common source of recurring oral ulcerations is the herpes simplex virus (HSV-1). Oral ulcerations
also result from infection by other viruses, including the HIV,
Coxsackie and ECHO viruses. Fungal and bacterial infections associated with oral ulcers are rarer and require extra
consideration with respect to immunocompromised status.8
Other ulcerative conditions include oral squamous cell carcinoma (SCC) and trauma-related lesions (thermal, chemical or
physical). Prescribed medications are also associated with the
development of oral ulcers. Extensive mucositis and stomatitis are seen in patients following head and neck radiation and
chemotherapy. Systemic conditions involving oral ulcerations
2
Major aphthous ulcers
Major aphthae (Sutton’s ulcers) are more severe than minor aphthae — larger, slower to heal and more painful — and can lead
to adjacent and facial edema. They are found in all regions of
oral mucosa, including keratinized mucosa, and are often larger
than a centimeter in size. While they typically heal in ten to forty
days, in extreme cases healing can take months while new ulcers
are developing. Major RAU heal with scarring. If long-lasting
and frequently recurring, they can result in morbidity and poor
quality of life, with poor nutrition and stress.11,12
Herpetiform aphthous ulcers
Herpetiform ulcers occur as multiple lesions, up to 100 at a time,
and can range from <1 mm to 3 mm in diameter each. Herpetiform RAU also coalesce into larger irregular lesions. Healing
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Figure 2. Major aphthous ulcer
Figure 3. Herpetiform aphthous ulcers
usually occurs in seven to ten days, without any scarring. Herpetiform ulcers do not exhibit a vesicle stage and are not infectious.
Etiology of Oral Ulcerations
The exact etiology of RAU is not known. Systemic and local factors, as well as infectious agents, have been proposed. Medications including nonsteroidal anti-inflammatory drugs (NSAIDs);
hypertensive medications such as ACE inhibitors, beta-blockers
with alpha-blocking activity and calcium channel blockers; and
cyclosporine, interferons, penicillin, sulfonamides and nicorandil
have all been implicated in oral ulcerations.13,14 ,15,16,17,18,19
Systemic Factors and Conditions
Genetic factors
More than 40% of patients with RAU may have a family history of these ulcers.20 Patients with a positive family history
tend to develop oral ulcers at an earlier age and have more
symptoms than do other individuals.21,22 Genetically specific
antigens, called human leukocyte antigen (HLA) subtypes,
have been identified in patients with RAU; however, no definitive association has been shown.23,24
Syndromes and conditions
Systemic conditions associated with RAU include Behçet’s
disease, MAGIC disease, Sweet’s syndrome, inflammatory intestinal diseases and immunological factors. Behçet’s
disease is characterized by recurrent oral, ocular and genital
ulcers and includes vascular, central nervous system and gastrointestinal involvement. Of patients with Behçet’s disease,
99% experience oral aphthae.25 MAGIC disease includes oral
and genital ulcers and cartilage inflammation.26 Sweet’s synwww.ineedce.com
drome often presents with classic RAU in addition to fever,
erythematous skin lesions and neutrophil disorder.27
Gastrointestinal diseases associated with RAU include
celiac disease and Crohn’s disease. Celiac disease (also known
as celiac sprue or gluten-sensitive enteropathy) is characterized by nutrient malabsorption and improves as gluten is
withdrawn from the diet. The most common oral symptom is
RAU. A recent study revealed that as many as 42% of celiac
disease patients screened had oral soft tissue ulcerations, compared with 2% of the control group.28 With Crohn’s disease,
RAU are the common oral manifestation; in a prospective
study of 792 patients, RAU occurred in 10.6% of patients with
the incidence slightly higher than with ulcerative colitis.29
Oral ulcers have been seen in 25%–45% of systemic lupus
erythematosis (SLE) patients.30 SLE-related lesions are more
apt to be on the hard palate and often improve with the treatment of other systemic and cutaneous SLE manifestations.31
Other conditions associated with oral ulcerations include
(but are not limited to) mucous membrane pemphigoid, pemphigus vulgaris, Reiter’s syndrome and erythema multiforme.
Immunologic factors
Some studies have suggested that RAU is a result of an abnormal immune response. Increased concentrations of neutrophils
in the ulcerative phase of the lesion suggest an active role in the
pathogenesis or healing of RAU.32,33 Mast cells are able to release
a variety of mediators, including cytokines and proteinases, and
have been shown to be 63% more numerous in RAU than in
healthy mucosa.34 A decreased ratio of CD4 to CD8 T-lymphocytes has also been reported.35 Further research is needed to better understand the relationship of RAU to immunoregulation.
Hematinic deficiencies
The prevalence of iron, folic acid and B12 deficiencies and
their role in RAU is not well understood. In recent studies,
patients with RAU were found to have more hematinic deficiencies than did the control group, with low-serum vitamin
B12 being the most common deficiency.36,37
Neutropenia
Neutropenia is characterized by an abnormally low count
(<1,500 cells/mm³) of neutrophils in the peripheral blood. It is
often associated with clinical AIDS and lower CD4 cell counts,
and the risk for bacterial infection is a concern.38 Neutropenic
ulcerations are often severe and can appear on the keratinized
and nonkeratinized tissue, and if the neutrophil count is not
restored to normal, resolution is not as successful.39,40
Hormonal
The appearance of RAU may coincide with the menstrual
cycle in a minority of women, but studies are contradictory.41,42 In a review of the literature, no association could
be determined from existing studies between RAU and the
premenstrual period, pregnancy or menopause.43
3
Stress
Early studies associated RAU with anxiety and emotional
stress.44 Higher incidences of RAU have been found among
patients suffering from psychological disorders45 and in patients with genetic defects linked to increased anxiety traits.46
Clinical assessment should at least consider the role of stress
in the appearance of RAU.
Bacterial and Viral Factors
Bacterial agents
A recent study using DNA sequencing found 95 bacterial
species in RAU,47 with only three species or phylotypes common to both the RAU and control groups. Prevotella was
found only in RAU samples, and the RAU group showed
greater bacterial diversity. In early studies, streptococci were
implicated as a possible cause for RAU,48 but further study
has not been able to confirm this relationship.49 Helicobacter
pylori has been found in up to 72% of RAU,50 but a link to
RAU is considered unlikely.51 Tuberculosis and syphilis
have also been found to be associated with oral ulcerations
in rare cases.52
Food hypersensitivities
Histamine release to food antigens has been reported in RAU
patients.61 RAU patients have reported a correlation between
the onset of lesions and the consumption of walnuts, tomatoes
and strawberries. Subsequent testing of these patients failed
to identify any significant causation relationship between
food hypersensitivity and RAU. However, this study did not
utilize skin prick tests or patch tests to determine hypersensitivity.62 One study using patch tests reported that, in RAU
patients testing positive to benzoic acid and cinnamaldehyde,
a more than 80% decrease in the frequency of RAU was found
with avoidance of the allergen,63 and in other studies specific
food avoidance resulted in similar results.64,65
Trauma
Patients predisposed to RAU develop lesions at sites of
trauma.58 It is important to note that not all trauma leads to
RAU, and many patients with RAU do not develop lesions
after trauma.59 A recent population-based study of American
adults did not find any significant association of trauma, such
as cheek or lip bite, with RAU.60
Sodium lauryl sulfate (SLS)
Sodium lauryl sulfate (SLS) has been implicated as a factor
in the development of RAU. SLS is the most frequently
used detergent and surfactant in commercially available
dentifrices and mouthwashes. SLS-susceptible (or sensitive) individuals were found to have severe skin reactions
and irritation to four commercial dentifrices containing
SLS, indicating that such individuals should avoid these
products.66 It has been proposed that SLS may denature the
mucosal mucin layer, which then exposes the oral epithelium to irritating agents and allergens, making the patient
more susceptible to RAU.67,68 This undesirable effect is not
due to any increased oral retention of SLS, as the contact
time of retained SLS is minimal.69 Studies reveal that use
of dentifrices with 0.5%, 1.0% and 1.5% SLS resulted in
significantly more epithelial desquamation than is seen with
SLS-free dentifrices.70,71 Premenopausal women react more
to SLS-containing dentifrices than do their postmenopausal
counterparts.72 In one study, the incidence of RAU was reduced by 81% when an SLS-free dentifrice was used instead
of an SLS-containing dentifrice;73 however, a second study
found no difference in the frequency or severity of RAU in
people using SLS-containing versus SLS-free dentifrice.74
In a 6-week test, xerostomic patients showed no increase in
RAU when using a dentifrice containing 1% SLS.75
In a recent in vitro study of reconstructed human oral
mucosa, a dual biological effect was demonstrated with SLS.76
Progressive desquamation and cell death prevailed at concentrations of SLS ranging from >0.15% to 1.5%. Compared
to previous studies that supported the destructive effects
of SLS,77,78 this study observed a protective mucosal effect
induced by a low SLS concentration (0.015%). Based on this
in vitro study and existing data, more studies are indicated to
develop less-irritating products for patient home care.
Squamous cell carcinoma
Oral squamous cell carcinoma (SCC) is often asymptomatic
until advanced. One presentation of SCC is as an ulcer that
does not heal. It is essential to consider this, given the morbidity and mortality associated with oral cancer.
Other chemicals
Chemicals have been implicated in oral ulcerations. Painful
hydrogen peroxide burns appearing as focal areas of ulceration have been reported.79 Gingival irritation and sensitivity are side effects of tooth bleaching and are resolved a few
Viral agents
Viruses may play a role in oral ulceration by eliciting an
immune response. Viruses associated with oral ulcerations
include human herpes virus-8 (HHV-8), cytomegalovirus
(CMV), Epstein-Barr virus (EBV), human papilloma virus
(HPV) and herpes simplex virus (HSV-1). Some of these
viruses may be solely responsible for oral ulceration, while
others require a co-infection of two or more viruses to induce
ulceration.53 Oral manifestations of measles have been seen in
20% of patients affected.54,55 HIV results in oral ulcerations
including (but not limited to) RAU. Severe episodes of RAU
are seen in HIV-infected patients. Unlike RAU that affect the
general population, RAU in HIV-infected patients tend to
be larger, last longer (weeks or months in some cases) and be
more resistant to treatment.56,57
Local Factors and Conditions
4
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days following discontinuation of use.80,81 A high-alcohol
oromucosal spray was shown to cause painful oral ulcers
that resolved when use was discontinued.82 High-alcohol
mouthwashes have also been associated with oral ulcerations,
but the appearance of the associated ulcers is not typical of
RAU.83 Flavoring, preservatives and coloring agents are common allergens in dentifrices and may cause contact stomatitis
on the oral mucosa.84 Tartar control toothpastes with pyrophosphates may also contribute to irritation, ulcerations and
gingival sensitivity in certain patients.85,86
Table 1. Etiological factors of oral ulcerations
Systemic
Genetics
Local
Trauma
Inflammatory bowel disease
Chemical
Crohn’s disease
SLS
Celiac disease
Cinnamaldehyde
Ulcerative colitis
Pyrophosphates
Drug reactions
Alcohol
Hematinic deficiencies
Hydrogen/carbamide
peroxide
Leukemia
Food additive sensitivities
Anemia
Foods
Neutropenia
SCC
Viral
Immunologic factors
Behçet’s disease
HIV
MAGIC disease
Herpes simplex, human and
zoster
Sweet’s syndrome
Epstein-Barr virus
PFAFA
Human papilloma virus
Mucous membrane pemphigoid
Cytomegalovirus
Pemphigus vulgaris
ECHO virus
Erythema multiforme
Coxsackie virus
Bacterial
Lichen planus
Hormonal
Prevotella
Stress
Tuberculosis
Inverse relationship to smoking
Syphilis
Tobacco
There is an inverse relationship between tobacco use, including smokeless tobacco, and RAU. In smokeless tobacco, this
negative association may be related to increased keratinization
of the oral mucosa, especially in the area where the tobacco is
held.87 It has been suggested that nicotine may affect the immune response. In a case study of nonsmokers suffering from
RAU, chewable nicotine (2–8 mg) gum tablets were administered for one month. In all cases there was remission, but after
treatment was discontinued the RAU reappeared.88
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Differential Diagnosis
A medical and dental history, intraoral and perioral examination, and examination of the cervical lymph nodes are all
required. It is worthwhile to review the history with the patient and ask specific questions related to possible etiologies
(Table 2). Patients may wrongly assume that other problems
are unrelated, not worth mentioning or too embarrassing, and
therefore may not note them on the medical history form.
Table 2. Patient history review questions for oral ulcerations
•
•
•
•
•
•
•
•
•
How long have you had this ulcer?
Have you had this before? When? How many? Where?
Has anything changed recently?
Have you stopped smoking recently?
Have you changed your toothpaste? What are you using?
Do you notice the ulcers after eating certain foods?
Do you get ulcers on other areas of your skin or body?
Do you have inflammatory bowel disease?
Is there anything else you feel you should add?
In many cases, the medical history and examinations described above may be all that is required for a definitive diagnosis
of RAU. Also ascertain if the patient recently stopped smoking,
as this results in an increased incidence of RAU.89 This is not to
suggest that patients should resume tobacco habits.
The most common ulcers to be mistaken for RAU are
recurring intraoral herpes lesions. Recurring intraoral herpes
lesions are similar to RAU but have important differences. If
recurrences are common and the appearance is one of multiple
tiny vesicles, typically <1 mm in diameter, and the lesions are
located on keratinized tissue (attached gingivae, hard palate)
or the vermilion border, the diagnosis is likely recurrent herpetic lesions.90 The vesicles may also rupture and coalesce. If
a red halo is present, it is scalloped, not smooth as in RAU.91
Recurrent herpes lesions may also be accompanied by malaise, fever, joint pain and cervical lymphadenopathy. Fever is
rare with RAU and would suggest a different diagnosis.
Trauma-induced ulcers may mimic RAU in appearance,
however usually they can be linked to a traumatic incident
such as lip-biting (Figure 5).
If the patient has genital and/or ocular ulcers and lesions
as well as RAU, this is suggestive of Behçet’s disease, and
for 67% of patients oral aphthae are the first sign and symptom.92,93 Genital and oral ulcers, when also involving inflammation of cartilage, are suggestive of MAGIC syndrome.94
RAU and ocular lesions are also found in benign mucous
membrane pemphigoid (Figure 6). A patient with skin lesions may require investigation for a variety of conditions,
including Sweet’s syndrome, pemphigus vulgaris (Figure 7),
and fungal and bacterial infections. Careful elicitation of the
medical history (particularly concerning diarrhea) may suggest investigation for inflammatory bowel disease, if it is not
already diagnosed. Of RAU patients, 5% have been found to
suffer from celiac disease.95,96 Oral symptoms precede intestinal symptoms in about 60% of the cases of Crohn’s disease.97
5
Figure 4. Intraoral
herpes lesions
Figure 5. Trauma-induced ulcer following lip biting
Single lesions that do not heal within 2 weeks (including following removal of a traumatic irritant), particularly
if there is no previous history of similar lesions, should be
viewed with suspicion. The differential diagnosis must
include squamous cell carcinoma (SCC), and a definitive
biopsy may be required (Figure 8).
Patients with long-lasting RAU that are particularly severe
and refuse to heal are suspect for HIV infection or another immunocompromised condition. RAU in these patients are more
severe, are of long duration, heal poorly and are debilitating.98
In cases of frequent or severe outbreaks of RAU, a referral
for systemic disease and vitamin deficiency screening should
be given, if such conditions were not previously diagnosed.
Sensitivity screening may also be considered to rule out reactions to foods and chemicals such as SLS.
Palliative Care
There is no definitive cure for aphthous ulcers. Palliative care
can be provided to relieve pain, promote healing and prevent
secondary infection. Various topical and systemic medications are available.
Figure 6a. Intraoral ulcer associated with benign mucous
membrane pemphigoid
Figure 6b. Ocular lesion associated with benign mucous
membrane pemphigoid
If patients have skin, ocular, genital or other non-oral
mucosal lesions, the diagnosis is unlikely to be RAU unless
there are coincidental one-time unrelated lesions. Similarly,
the diagnosis is unlikely to be RAU if fever is present.
6
Topical medications
Pain-relieving topical gels that can be dabbed on the lesion
include 2% lidocaine and 20% benzocaine-based products
(Colgate® Orabase®, Orajel® Ultra, Anbesol®). Lidocaine
mouth rinse or spray can also be used. Topical pain-relieving
barrier agents that have been shown to promote healing include octylcyanoacrylate (Soothe-N-Seal™)99 and 5% amlexanox paste (Aphthasol®).100,101 5% amlexanox paste can reduce
the severity of ulcers if applied two to four times daily in the
initial phase of ulcer development. Rinses that form a bioadherent protective mucosal coating are available (Rincinol®,
Gelclair®); these are useful if lesions are widespread.
Topical corticosteroids are available in varying potencies.
Topical hydrocortisone hemisuccinate pellets (2.5 mg) can be
used for nonsevere cases.102 Triamcinolone acetonide paste
(Kena­log in Orabase®) is a medium-potency prescription
topical corticosteroid that helps to reduce pain, inflammation
and ul­cera­tion when applied two or three times daily for five
days. An alternative is fluocinonide dental paste (Lidex in
Orabase).103 Four to five days’ use of tetracycline or minocycline rinse four times daily has also been found to be helpful in
treating RAU. Tetracycline rinse can be made using a 250 mg
capsule dissolved in 180 cc water.104 These rinses should not
be used in young children because of the risk of intrinsic staining in developing teeth should the child swallow the rinse.
For severe RAU, higher potency anesthetic rinses, topical
corticosteroids, tetracycline and/or systemic medications are
needed. Palliative rinses combining equal parts 2% lidocaine,
a bioadhesive coating agent (such as kaopectate) and an antihistamine are effective. Betamethasone mouth rinse is more
effective than are hydrocortisone and triamcinolone rinses.
However, there is a risk of opportunistic candidal infections,
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Figure 7a. Oral ulcerations in a pemphigus patient
Table 3. Topical medications
Mild and moderate RAU
2% lidocaine
Hydrocortisone hemi succinate
20% benzocaine
Triamcinalone acetonide
Cyanoacrylate
Fluocinonide
5% amlexanox
Tetracycline/minocyline rinses
Rincinol
L-lysine
Gelclair
Zinc lozenges
Severe RAU
Figure 7b. Skin lesions in pemphigus patient
Combination rinses
á-interferon rinse
Betamethasone rinse
Table 4. Additional care
Figure 8. Squamous cell carcinoma
Nutritional
Other
Vitamins
Elimination of food allergens
Non-spicy food and drink
Elimination of gluten (Celiac’s)
Adequate fluid intake
Reduced dose SLS dentifrice
Oral Hygiene
SLS-free dentifrice
Ultra soft toothbrush
Elimination of other chemicals
Adjunctive rinsing
Drug reactions —
discontinue drugs
Remove sharp points
become pregnant, as it is a potent teratogen. Other systemic
medications have also been used. Alternative therapies, such
as bee propolis (500mg/day), show promise in reducing the
number of recurrences of RAU.113
Courtesy of Denis P. Lynch, DDS, PhD
and a greater risk for adrenal suppression with long-term use.105
If long-term use of topical corticosteroids is necessary, antifungal lozenges or mouth rinses may be required to help prevent
candidiasis. An á-interferon rinse — an immunomodulator —
may also be effective in treating severe cases of RAU.106
Systemic medications
Systemic medications may be required for the most severe
cases. Prednisone (60 mg) four times daily for five to seven
days is effective; its use should be avoided in HIV-infected
and other immunocompromised patients. If prednisone is
used for longer than seven days, slow tapering off is required
due to adrenal suppression. For focally severe resistant ulcers,
a local triamcinalone injection into the lesion may help.107
For refractory cases, thalidomide (200 mg four times daily
for four weeks), dapsone, colchicine and pentoxifylline may
be helpful.108,109,110 Colchicine administered three times
daily (0.5 mg) over two months has been found to decrease
the number of ulcers and to reduce pain.111,112 Thalidomide
must never be used in pregnant women or women who may
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Nutrition and oral hygiene
Aphthae make eating and drinking painful. Patients should
avoid hard or crunchy foods and snacks, spicy and salty foods,
hot drinks, and acidic drinks (such as orange juice). Using a
straw or sipping liquid slowly will help, as will eating soft, bland
foods. Patients must drink an adequate amount of fluid.114
Sipping cold, nonacidic drinks may also help soothe lesions.
Maintaining oral hygiene, in addition to its usual benefits,
helps prevent secondary infection. Patients should use an ultrasoft toothbrush. Adjunctive use of chlorhexidine gluconate
or cetylpyridinum chloride mouth rinse helps reduce the bacterial load and plaque while patients are having difficulty brushing.115 Twice-daily rinsing with 0.12% chlorhexidine gluconate
can increase the number of days without ulcers, although it has
not been found to influence the incidence or severity of RAU.
If vitamin deficiencies are present, supplements can be given.
RAU patients have been shown to respond to B12 replacement
therapy.116 Sharp areas on the dentition or restorations should
be smoothed to help prevent trauma if a lesion is present and to
help reduce pain during eating and drinking.
While discontinuation of medications associated with oral
ulcers is indicated to prevent oral ulcers, such discontinuation
7
may be medically contraindicated if an alternative is not available. In these cases, aggressive management and palliative
care of oral ulceration is essential.
Sensitivities
Strict elimination diets for food sensitivities have shown significant improvement and/or resolution of persistent lesions
in 40%–80% of patients, but patient dropout rates in these
studies raise concerns about compliance.117,118,119 Also of note
is that 89% of celiac disease patients have been found to have
no RAU after one year on a gluten-free diet.120
SLS-related sensitivities may be dose-related rather than absolute. For patients with such sensitivities, use of SLS-free oral
care products or those with reduced SLS is recommended.121
Summary
Oral ulcerations are a common condition, with RAU being
the most common. It is important to be able to perform an accurate differential diagnosis to ensure that the patient receives
the appropriate treatment. RAU include minor, major and
herpetiform variants that differ in size, location, duration, and
level of discomfort or pain. Possible etiologies include systemic
and local conditions as well as food and chemical sensitivities.
RAU are treated palliatively with a variety of topical and
systemic medications, the selection of which is based on the
individual patient’s needs and on the severity of the ulceration.
In cases where allergic responses to food or food additives are
involved, the patient should avoid those foods. Patients who
have suspected or confirmed SLS sensitivity should use a dentifrice containing either no SLS or a low level of SLS.
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9 Ibid.
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15 Barrons, RW. Treatment strategies for recurrent oral aphthous ulcers. Am J Health-Syst Pharm.
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16 Göker E, Rodenhuis S. Early onset of oral aphthous ulcers with weekly docetaxel. Neth J Med.
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17 Abdollahi A, Radfar M. A review of drug-induced oral reactions. J Contemp Dent Pract.
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18 Boulinguez S, Reix S, Bedane C, et al. Role of drug exposure in aphthous ulcers: a case-control
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8
19 Scully C, Felix DH. Oral medicine – Update for the dental practitioner. Aphthous and other common
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20 Ship II. Inheritance of aphthous ulcers of the mouth. J Dent Res. 1965; 44:837–44.
21 Ship JA. Recurrent aphthous stomatitis: An update. Oral Surg Oral Med Oral Pathol. 1996;
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22 Lake RI, Thomas SJ, Martin NG. Genetic factors in the aetiology of mouth ulcers. Genet. Epidemiol.
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23 Challacombe SJ, Batchelor JR, Kennedy LA, Lehner T. HLA antigens in recurrent oral ulcerations.
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24 Shohat-Zabarski R, Kalderon S, Klein T, Weinberger A, Tikva P, Aviv R. Close association of HLA-B51 in
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25 Lehner T. Oral ulceration and Behçet’s syndrome. Gut. 1977;18:491–511.
26 Porter SR, Scully C, Pedersen A. Recurrent aphthous stomatitis. Crit Rev Oral Biol Med.
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27 Notani K, Kobayashi S, Kondoh K, Shindoh M, Ferguson MM, Fukuda H. A case of Sweet’s syndrome
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28 Campisi G, Di Liberto C, Iacono G, Compilato D, Di Prima L, et al. Oral pathology in untreated coeliac
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29 Burgan SZ, Sawair FA, Amarin ZO. Hematologic status in patients with recurrent aphthous
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31 McCauliffe DP. Cutaneous Lupus Erythematosus. Semin Cutan Med Surg. 2001;20(1):14–26.
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33 Wray D, Charon J. Polymorphonuclear neutrophil function in recurrent aphthous stomatitis. J Oral
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34 Natah SS, Hayrinen-Immonen R, Heitanen J, Malstrom M, Konttinen YT. Quantitative assessment
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35 Bachtiar EW, Cornain S, Siregar B, Raharjo TW. Decreased CD4+/CD8+ ratio in major types of
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36 Burgan SZ, Sawair FA, Amarin ZO. Hematologic status in patients with recurrent aphthous
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38 Levine AM, Ervin CM, Gange SJ, Anastos K, Young M, et al. Neutropenia in human
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39 Porter SR, Scully C, Standen GR. Autoimmune neutropenia manifesting as recurrent oral ulceration.
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40 Luzzi GA, Jones BJ. Treatment of neutropenic oral ulceration in human immunodeficiency virus
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41 Dolby AE. Recurrent Mikulicz’s oral apthae. Their relationship to the menstrual cycle. Br Dent J.
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42 Segal AL, Katcher AH, Brightman VJ, Miller MF. Recurrent herpes labialis, recurrent aphthous ulcers
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43 McCartan BE, Sullivan A. The association of menstrual cycle, pregnancy, and menopause with
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44 Ship I, Morris AL, Durocher RT, Burket LW. Recurrent aphthous ulcerations in a professional school
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45 Soto-Araya M, Rojas AG, Esguep A. Association between psychological disorders and the presence
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46 Victoria JMN, Correia-Silva J, Pimenta FJ, Kalapothakis E, Gomez, RS. Serotonin transporter gene
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47 Marchini L, Campos MS, Sila AM, Paulino LC, Nobrega FG. Bacterial diversity in aphthous ulcers.
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48 Barile MF, Grayowski MD, Driscoll EJ, Riggs DB. L Form of bacteria isolated from recurrent aphthous
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49 Riggio MP, Lennon A, Ghodratnama F, Wray D. Lack of association between Streptococcus oralis and
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50 Birek C, Grandhi R, McNeill K, Singer D, Ficarra G, Bowden G. Detection of Helicobacter pylori in oral
aphthous ulcers. J Oral Pathol Med. 1999;28:197–203.
51 Iamaroon A, Chaimano S, Linpisarn S, Pongsiriwet S, Phornphutkul K. Detection of Heliobacter
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52 Scully C, Felix DH. Oral medicine – Update for the dental practitioner. Aphthous and other common
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53 Lin SS, Chou MY, Ho CC, Kao CT, Tsai CH, Wang L, Yang CC. Study of the viral infections and cytokines
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54 Guelmann KJ, Stavropolous F, Heft M. Gingival and other oral manifestations in measles virus
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55 Czerninski R, Katz J, Schlesinger M. Preliminary evidence for an association of measles virus
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56 Muzyka BC, Glick M. Major aphthous ulcers in patients with HIV disease. Oral Surg Oral Med Oral
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57 Youle M, Clarbour J, Farthing C, et al. Treatment of resistant aphthous ulceration with thalidomide
www.ineedce.com
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58 Wray D, Graykowski EA, Notkins AL. Role of mucosal injury in initiating recurrent aphthous
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59 Ross R, Kitscher AH, Zegarelli EV, PIro ID, Silvers H. Relationship of mechanical trauma to recurrent
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60 Chattopadhyay A, Chatterjee S. Risk indicators for recurrent aphthous ulcers among adults in the
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61 Wray D, Vlagopoulous TP, Siraganian RP. Food allergens and basophil histamine release in recurrent
aphthous stomatitis. Oral Surg Oral Med Oral Pathol. 1982;54(4):388–95.
62 Eversole LR, Shopper TP, Chambers DW. Effects of suspected foodstuff challenging agents in the
aetiology of recurrent aphthous stomatitis. Oral Surg Oral Med Oral Pathol. 1982;54(1):33–8.
63 Nolan A, Lamey PJ, Milligan KA, Forsyth A. Recurrent aphthous ulceration and food sensitivity. J
Oral Pathol Med. 1991;20:473–5.
64 Wright A, Ryan FP, Willingham SE, Holt S, Page AC, et al. Food allergy or intolerance in severe
recurrent aphthous ulceration of the mouth. Br Med J (Clin Res Ed). 1986; 292(6530):1237–8.
65 Hay KD, Reade PC. The use of an elimination diet in the treatment of recurrent aphthous ulceration
of the oral cavity. Oral Surg Oral Med Oral Pathol. 57(5):504–7.
66 Skaare AB, Kjaerheim V, Barkvoll P, Rölla G. Skin reactions and irritation potential of four commercial
toothpastes. Acta Odontol Scand. 1997;55(2):133–6.
67 Herlofson BB, Barkvoll P. Sodium lauryl sulfate and recurrent aphthous ulcers. A preliminary study.
Acta Odontol Scand. 1994;52: 257–9.
68 Chahine L, Sempson N, Wagoner C. The effect of sodium lauryl sulfate on recurrent aphthous
ulcers: A clinical study. Compend Cont Educ Dent. 1997;18(12):1238–40.
69 Fakhry-Smith S, Din C, Nathoo SA, Gaffar A. Clearance of sodium lauryl sulphate from the oral
cavity. J Clin Periodontol. 1997;24: 313–7.
70 Herlofson BB, Barvoll P. Oral mucosal desquamation caused by two toothpaste detergents in an
experimental model. Eur J. Oral Sci. 1996;104: 21–6.
71 Herlofson BB, Barkvoll P. Sodium lauryl sulfate and recurrent aphthous ulcers. A preliminary study.
Acta Odontol Scand. 1994;52:257–9.
72 Herlofson BB, Barkvoll P. Oral mucosal desquamation of pre- and postmenopausal women: A
comparison of response to sodium lauryl sulphate in toothpastes. J Clin Periodontol. 1996;23(6):
567–71.
73 Chahine L, Sempson N, Wagoner C. The effect of sodium lauryl sulfate on recurrent aphthous
ulcers: A clinical study. Compend Cont Educ Dent. 1997;18(12):1238–40.
74 Healy CM, Paterson M, Joyston-Bechal S, Williams DM, Thornhill MH. The effect of a sodium lauryl
sulfate–free dentifrice on patients with recurrent oral ulceration. Oral Dis. 1999;5:39–43.
75 Rantanen I, Tenovuo J, Pienihäkkinen K, et al. Effects of a betaine-containing toothpaste
on subjective symptoms of dry mouth, a randomised clinical trial. J Contemp Dent Pract.
2003;(4)2:11–23.
76 Neppelberg E, Costea DE, Vintermyr OK, Johannessen AC. Dual effects of sodium lauryl sulphate on
human oral epithelial structure. Exp Dermatol. 2007;16:574–9.
77 Skaare AB, Rölla G, Barkvoll P. The influence of triclosan, zinc or propylene glycol on oral mucosa
exposed to sodium lauryl sulphate. Eur J Oral Sci. 1997;105:527–33.
78 Healy CM, Cruchley AT, Thornhill MH, Williams DM. The effect of sodium lauryl sulphate, triclosan
and zinc on the permeability of normal oral mucosa. Oral Dis. 2000;15:801–07.
79 Shetty K. Hydrogen peroxide burns of the oral mucosa. Ann Pharm. 2006;40(2):351.
80 Leonard RH, Garland GE, Eagle JC, Caplan DJ. Safety issues when using a 16% carbamide peroxide
whitening solution. J Esthet Restorat Dent. 2002;14(6):358–67.
81 Leonard H, Smith LR, Garland GE, Tiwana KK, Zaidel LA, et al. Evaluation of Side Effects and Patients’
Perceptions during Tooth Bleaching. J Esthet Restorat Dent. 2007;19(6): 355–64.
82 Scully C. Cannabis: Adverse effects from an oromucosal spray. Br Dent J. 2007;203(6):336–7.
83 Touyz LZ, Hille JJ. A fruit-mouthwash chemical burn. Report of a case. Oral Surg Oral Med Oral
Pathol. 1984;58(3):290–2.
84 Sainio EL, Kanerva L. Contact allergens in toothpastes and a review of their hypersensitivity.
Contact Dermatitis. 1995;33(2):100–5.
85 Barsley RE, Cottone JA. The effects of tartar-control toothpaste on the oral soft tissues. Oral Surg
Oral Med Oral Pathol. 1990;70(4):529–36.
86 Delattre VF. Factors contributing to adverse soft tissue reactions due to the use of tartar control
toothpastes: Report of a case and literature review. J Periodontol. 1999;70(7):803–07.
87 Bittoun R. Recurrent aphthous ulcers and nicotine. Med J Aust. 1991;154:471–2.
88 Grady D, Ernster BL, Stillman L, Greenspan J. Smokeless tobacco use prevents aphthous stomatitis.
Oral Surg Oral Med Oral Pathol. 1992;74:463–5.
89 McRobbie H, Hajek P, Gillison F. The relationship between smoking cessation and mouth ulcers.
Nictoine Tob Res. 2004;6(4):655–59.
90 Sciubba JJ. Herpes simplex and aphthous ulcerations. Presentation, diagnosis and management.
Gen Dent. 2005;51:510–17.
91 Tilliss TSI, McDowell J. Differential diagnosis: Is it herpes or aphthous? J Cont Dent Pract. 2002;
3(1):
92 Lehner T. Immunological aspects of recurrent oral ulceration and Behçet’s syndrome. J Oral Pathol.
1978;7:424–30.
93 Lehner T. Oral ulceration and Behçet’s syndrome. Gut. 1977;18:491–511.
94 Porter SR, Scully C, Pedersen A. Recurrent aphthous stomatitis. Crit Rev Oral Biol Med.
1998;9(3):306–21.
95 Veloso FT, Saleiro JV. Small-bowel changes in recurrent ulceration of the mouth. Hepatogastroenterol.
1987;34:36–7.
96 Ferguson R, Basu MK, Asquith P, Cooke WT. Jejunal mucosal abnormalities in patients with
recurrent aphthous ulceration. Br Med J. 1976;1:11–3.
97 Rehberger A, Puspok A, Stallmeister T, Jureck W. Crohn’s disease masquerading as aphthous ulcers.
Eur J Dermatol. 1998;8(4):274–276.
www.ineedce.com
98 Muzyka BC, Glick M. Major aphthous ulcers in patients with HIV disease. Oral Surg Oral Med Oral
Pathol. 1994;77:116–20.
99 Gaffar A, Narang U, Kutcher M, et al. Oral first aid in the 21st century. Supplement to Compendium
of Continuing Education in Dentistry 2001;22(32):1–33.
100 Greer RO, Lindenmuth JE, Juarez T, Khandwala A. A double-blind study of topically applied 5%
amlexanox in the treatment of aphthous ulcers. J Oral Maxillofac Surg. 1993;51:243–9.
101 Binnie WH, Curro FA, Khandwala A, VanInwegan RG. Amlexanox oral paste: a novel treatment that
accelerates the healing of aphthous ulcers. Compend Cont Educ Dent 1997;18:1116–8,1120–2.
102 Scully C, Felix DH. Oral medicine—Update for the dental practitioner. Aphthous and other
common ulcers. Br Dent J. 2005;199:259–64.
103 Marinopoulos S. Apthous ulcers. Available at: http://www.hopkins-hivguide.org/diagnosis/
organ_system/heent/full_aphthous_ulcers.html. Accessed January 12, 2008.
104 Ibid.
105 Scully C, Felix DH. Oral medicine – Update for the dental practitioner. Aphthous and other common
ulcers. Br Dent J. 2005;199:259–64.
106 Altenburg A, Abdel-Naser MB, Seeber H, Abdallah M, Zouboulis CC. Practical aspects of management
of recurrent aphthous stomatitis. J Eur Acad Dermatol Venereol. 2007;21(8):1019–26.
107 Scully C, Gorsky M, Lozada-Nur F. The diagnosis and management of recurrent aphthous stomatitis.
A consensus approach. J Am Dent Assoc. 2003;134(2):200–7.
108 Marinopoulos S. Apthous ulcers. Available at: http://www.hopkins-hivguide.org/diagnosis/
organ_system/heent/full_aphthous_ulcers.html. Accessed January 12, 2008.
109 Eisen D, Lynch DP. Selecting topical and systemic agents for recurrent aphthous stomatitis. Cutis.
2001;68(3):201–6.
110 Jacobson JM, Greenspan JS, Spritzler J, et al. Thalidomide for the treatment of oral aphthous
ulcers in patients with human immunodeficiency virus infection. National Institute of Allergy and
Infectious Diseases AIDS Clinical Trials Group. N Engl J Med; 1997;336(1):487–93.
111 Gatot A, Tovi F. Colchicine therapy in recurrent oral ulcers. Arch Dermatol. 1984;120:994.
112 Katz J, Langevitz P, Shemer J, Barak S, Livneh A. Prevention of recurrent aphthous stomatitis with
colchicine: An open trial. J Am Acad Dermatol. 1994;31:459–61.
113 Samet N, Laurent C, Susarla SM, Samet-Rubinsteen N. The effect of bee propolis on recurrent
apthous stomatitis: a pilot study. Clin Oral Invest. 2007;11:143–7
114 Scully C, Felix DH. Oral medicine – Update for the dental practitioner. Aphthous and other common
ulcers. Br Dent J. 2005;199:259–64.
115 Ibid.
116 Volkov I, Rudoy I, Abu-Rabia U, Masalha T, Masalha R. Case report: Recurrent aphthous stomatitis
responds to vitamin B12 treatment. Can Fam Physician. 2005 June;51:844–45.
117 Wright A, Ryan FP, Willingham SE, Holt S, Page AC, Hindle MO, Franklin CD. Food allergy or
intolerance in severe recurrent aphthous ulceration of the mouth. Br Med J (Clin Res Ed).
1986;292(6530):1237–38.
118 Nolan A, Lamey PJ, Milligan KA, Forsyth A. Recurrent aphthous ulceration and food sensitivity. J
Oral Pathol Med. 1991;20:473–75.
119 Hay KD, Reade PC. The use of an elimination diet in the treatment of recurrent aphthous ulceration
of the oral cavity. Oral Surg Oral Med Oral Pathol. 57(5):504–07.
120 Campisi G, Di Liberto C, Iacono G, Compilato D, Di Prima L, et al. Oral pathology in untreated coeliac
disease. Aliment Pharmacol Ther. 2007;26(11–12):1529–36.
121 Marinopoulos S. Apthous ulcers. Available at: http://www.hopkins-hivguide.org/diagnosis/
organ_system/heent/full_aphthous_ulcers.html. Accessed January 12, 2008.
Author Profiles
Michelle Hurlbutt, RDH, BS.
Assistant Professor, Department of Dental
Hygiene, School of Dentistry, Loma Linda
University.
Lane Thomsen, DDS, MS.
Chairperson, Department of Oral Diagnosis, Radiology and Pathology, School of
Dentistry, Loma Linda University.
Disclaimer
The authors of this course have no commercial ties with the sponsors or the
providers of the unrestricted educational grant for this course.
Reader Feedback
We encourage your comments on this or any ADTS course. For your convenience, an
online feedback form is available at www.ineedce.com.
9
Questions
1. The most common oral ulcers
are _________.
a. Recurrent herpes lesions
b. Recurrent aphthous ulcers
c. HIV-related
d. none of the above
2. Recurrent aphthous ulcers occur
in approximately 20 percent of
the population.
a. True
b. False
3. The second most common
source of recurring oral
ulcerations is _________.
a. the herpes zoster virus
b. the Coxsackie virus
c. syphilis
d. the herpes simplex virus
4. Systemic conditions involving oral
ulcerations include _________.
a. inflammatory bowel disease
b. Behçet’s disease
c. HIV infection
d. all of the above
5. Minor aphthous ulcers are common
on the dorsum of the tongue and on
keratinized mucosa.
a. True
b. False
6. Minor aphthous ulcers present
clinically with _________.
a. vesicles
b. pseudomembranous grayish or
yellowish centers
c. grey borders
d. all of the above
7. Major aphthae _________ .
a. heal without scarring
b. occur in 5 percent of the population
c. are also known as Sutton’s ulcers
d. all of the above
8. Herpetiform ulcers _________.
a. occur as multiple lesions
b. can range from <1 mm to 3 mm in diameter
c. coalesce
d. all of the above
9. More than _________ of patients
with RAU may have a family history
of these ulcers.
a. 10 percent
b. 20 percent
c. 30 percent
d. 40 percent
10. In one study, as many as 32 percent
of celiac disease patients screened had
oral soft tissue ulcerations.
a. True
b. False
10
11. The most common hematinic
deficiency seen in patients with
recurrent aphthous ulcers has been
found to be _________.
a. vitamin B6
b. vitamin B12
c. vitamin C
d. none of the above
12. Neutropenic ulcerations
are mild and appear only on
nonkeratinized tissue.
a. True
b. False
13. Helicobacter pylori has been found
to be definitively associated with
recurrent aphthous ulcers.
a. True
b. False
21. Oral ulcerations and skin lesions are
found in _________.
a. pemphigus vulgaris
b. Sweetener syndrome
c. fungal and bacterial infections
d. a and c
22. In cases of severe outbreaks of RAU,
a referral for systemic disease and
vitamin deficiency screening should
be given.
a. True
b. False
23. Recurrent aphthous ulcers
can be treated with topical and
systemic medications.
a. True
b. False
14. A recent population-based study of
American adults found _________.
24. Five percent amlexanox can reduce
the severity of ulcers if applied
_________ in the initial phase of
ulcer development.
15. Histamine release to food antigens
has been reported in RAU patients.
25. Pain-relieving topical gels containing _________ can be dabbed
on oral ulcerations.
a. a significant association of trauma with RAU
b. no significant association of trauma with RAU
c. all smokers develop RAU
d. a and c
a. True
b. False
16. Sodium lauryl sulfate (SLS) has
been implicated as a factor in the
development of RAU.
a. True
b. False
17. Use of dentifrices with 0.5 percent,
1.0 percent and 1.5 percent SLS in
studies resulted in _________.
a. significantly less epithelial desquamation than
is seen with SLS-free dentifrices
b. significantly more epithelial desquamation
than is seen with SLS-free dentifrices
c. no differences in the amount of epithelial
desquamation seen compared to with SLSfree dentifrices
d. oral malodor reduction
18. One in vitro study found a protective mucosal effect induced by a low
SLS concentration.
a. True
b. False
19. Common allergens in dentifrices
that may cause contact stomatitis on
the oral mucosa include _________.
a. flavorings
b. preservatives
c. coloring agents
d. all of the above
20. Oral ulcerations and ocular lesions
are found in _________.
a. benign mucous membrane pemphigoid
b. Behçet’s disease
c. MAGIC syndrome
d. all of the above
a. one to two times daily
b. two to four times daily
c. two to three times weekly
d. none of the above
a. 1% lidocaine and 10% benzocaine
b. 2% lidocaine and 15% benzocaine
c. 2% lidocaine and 20% benzocaine
d. 20% lidocaine and 2% benzocaine
26. If long-term use of topical corticosteroids is necessary, antifungal
agents may be required to help
prevent candidiasis.
a. True
b. False
27. For severe refractory cases
of recurrent aphthous ulcers,
_________ may be helpful.
a. colchicine
b. thalidomide
c. dapsone
d. all of the above
28. Discontinuation of medications
associated with oral ulcers is
always indicated.
a. True
b. False
29. For patients with sensitivities to
SLS, _________.
a. use of SLS-free oral care products
is recommended
b. use of oral care products with reduced
SLS is recommended
c. use of oral care products with cinnamaldehyde
instead is recommended
d. a and b
30. The selection of which medication to use to treat a patient’s
recurrent aphthous ulcers is based
on _________.
a. the severity of the ulcer
b. random selection
c. that patient’s individual needs
d. a and c
www.ineedce.com
ANSWER SHEET
Demystifying Recurrent Oral Ulcerations
Name:
Title:
Address:
E-mail:
City:
State:
Telephone: Home (
)
Office (
Specialty:
ZIP:
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Requirements for successful completion of the course and to obtain dental continuing education credits: 1) Read the entire course.2)
Complete all information above. 3) Complete answer sheets in either pen or pencil. 4) Mark only one answer for each question. 5) A score
of 70% on this test will earn you 4 CE credits. 6) Complete the Course Evaluation below. 7) Make check payable to The Academy of Dental
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Educational Objectives
Mail completed answer sheet to
Academy of Dental Therapeutics and Stomatology
P.O. Box 116, Chesterland, OH 44026
or fax to: (440) 845-3447
1. Explain the etiology of oral ulcerations.
2. Describe the clinical features and symptoms of aphthous ulcers.
3. Conduct a differential diagnosis for recurrent oral ulcerations.
4.Outline the topical and systemic medications used in the treatment of recurrent aphthous ulcerations and other palliative
care and recommendations for patients.
For immediate results, go to www.ineedce.com
and click on the button “Take Tests Online.” Answer
sheets can be faxed with credit card payment to
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P ayment of $59.00 is enclosed.
(Checks and credit cards are accepted.)
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Please evaluate this course by responding to the following statements, using a scale of Excellent = 5 to Poor = 0.
1. Were the individual course objectives met?Objective #1: Yes No
Objective #3: Yes No
Objective #2: Yes No
Objective #4: Yes No
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Exp. Date: _____________________
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10. If any of the continuing education questions were unclear or ambiguous, please list them.
___________________________________________________________________
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___________________________________________________________________
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AGD Code 739
PLEASE PHOTOCOPY ANSWER SHEET FOR ADDITIONAL PARTICIPANTS.
AUTHOR DISCLAIMER
The authors of this course have no commercial ties with the sponsors or the providers of
the unrestricted educational grant for this course.
SPONSOR/PROVIDER
This course was made possible through an unrestricted educational grant from Tom’s
of Maine. No manufacturer or third party has had any input into the development of
course content. All content has been derived from references listed, and or the opinions
of clinicians. Please direct all questions pertaining to the ADTS or the administration
of this course to Machele Galloway, 1421 S. Sheridan Rd., Tulsa, OK 74112 or
[email protected].
COURSE EVALUATION and PARTICIPANT FEEDBACK
We encourage participant feedback pertaining to all courses. Please be sure to complete the
survey included with the course. Please e-mail all questions to: [email protected].
www.ineedce.com
INSTRUCTIONS
All questions should have only one answer. Grading of this examination is done
manually. Participants will receive confirmation of passing by receipt of a certificate.
Certificates will be mailed within two weeks after taking an examination.
EDUCATIONAL DISCLAIMER
The opinions of efficacy or perceived value of any products or companies mentioned
in this course and expressed herein are those of the author(s) of the course and do not
necessarily reflect those of the ADTS.
Completing a single continuing education course does not provide enough information
to give the participant the feeling that s/he is an expert in the field related to the course
topic. It is a combination of many educational courses and clinical experience that
allows the participant to develop skills and expertise.
COURSE CREDITS/COST
All participants scoring at least 70% (answering 21 or more questions correctly) on
the examination will receive a certificate verifying 4 CE credits. The formal continuing
education program of this sponsor is accepted by the AGD for Fellowship/Mastership
credit. Please contact ADTS for current term of acceptance. Participants are urged to
contact their state dental boards for continuing education requirements. The ADTS is a
California Provider. The California Provider number is 3274. The cost for courses ranges
from $49.00 to $110.00.
Many ADTS self-study courses have been approved by the Dental Assisting National
Board, Inc. (DANB) and can be used by dental assistants who are DANB Certified to
meet DANB’s annual continuing education requirements. To find out if this course or any
other ADTS course has been approved by DANB, please contact DANB’s Recertification
Department at 1-800-FOR-DANB, ext. 445.
RECORD KEEPING
The ADTS maintains records of your successful completion of any exam. Please contact our
offices for a copy of your continuing education credits report. This report, which will list
all credits earned to date, will be generated and mailed to you within five business days
of receipt.
CANCELLATION/REFUND POLICY
Any participant who is not 100% satisfied with this course can request a full refund by
contacting the Academy of Dental Therapeutics and Stomatology in writing.
© 2007 by the Academy of Dental Therapeutics and Stomatology
NAT0803RDH
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